3.4.24.86 Acidosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25085885&form=6&db=m Hypercapnia attenuates ventilator-induced lung injury via a disintegrin and metalloprotease-17. causal interaction,ongoing research,therapeutic application,unassigned 2,3,1,0 3.4.24.86 Acute Kidney Injury http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27642633&form=6&db=m ADAM17 substrate release in proximal tubule drives kidney fibrosis. unassigned - 3.4.24.86 Acute Kidney Injury http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33153216&form=6&db=m Novel Evidence of Acute Kidney Injury in COVID-19. causal interaction,ongoing research,unassigned 4,2,0 3.4.24.86 Acute Lung Injury http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19295482&form=6&db=m Effects of tumor necrosis factor-a converting enzyme inhibition on acute lung injury induced by endotoxin in the rat. ongoing research,therapeutic application,unassigned 4,2,0 3.4.24.86 Acute Lung Injury http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21603616&form=6&db=m Leukocyte ADAM17 regulates acute pulmonary inflammation. causal interaction,ongoing research,therapeutic application,unassigned 4,4,3,0 3.4.24.86 adam 17 endopeptidase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16735599&form=6&db=m ADAM17 deficiency by mature neutrophils has differential effects on L-selectin shedding. causal interaction,unassigned 2,0 3.4.24.86 adam 17 endopeptidase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18722532&form=6&db=m Isoform-specific contribution of protein kinase C to prion processing. causal interaction,unassigned 4,0 3.4.24.86 adam 17 endopeptidase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20976004&form=6&db=m ADAM17 deletion in thymic epithelial cells alters aire expression without affecting T cell developmental progression. unassigned - 3.4.24.86 adam 17 endopeptidase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21828049&form=6&db=m Shedding of the MER tyrosine kinase receptor is mediated by ADAM17 through a pathway involving reactive oxygen species, protein kinase {delta}, and P38 map kinase. ongoing research,unassigned 2,0 3.4.24.86 adam 17 endopeptidase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23584255&form=6&db=m Macrophage ADAM17 deficiency augments CD36-dependent apoptotic cell uptake and the linked anti-inflammatory phenotype. causal interaction,unassigned 2,0 3.4.24.86 adam 17 endopeptidase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24135057&form=6&db=m Short-term TNF? shedding is independent of cytoplasmic phosphorylation or furin cleavage of ADAM17. diagnostic usage,therapeutic application,unassigned 3,1,0 3.4.24.86 adam 17 endopeptidase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24342803&form=6&db=m Smooth muscle cells relay acute pulmonary inflammation via distinct ADAM17/ErbB axes. causal interaction,ongoing research,unassigned 1,2,0 3.4.24.86 adam 17 endopeptidase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25108021&form=6&db=m The role of metalloproteinase ADAM17 in regulating ICOS ligand-mediated humoral immune responses. causal interaction,therapeutic application,unassigned 3,1,0 3.4.24.86 adam 17 endopeptidase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26683521&form=6&db=m Cytokine secretion and NK cell activity in human ADAM17 deficiency. causal interaction,ongoing research,unassigned 3,2,0 3.4.24.86 adam 17 endopeptidase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27077118&form=6&db=m Epithelial Cell-Derived a Disintegrin and Metalloproteinase-17 Confers Resistance to Colonic Inflammation Through EGFR Activation. causal interaction,ongoing research,therapeutic application,unassigned 4,4,2,0 3.4.24.86 adam 17 endopeptidase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28062509&form=6&db=m Adam17 Deficiency Promotes Atherosclerosis by Enhanced TNFR2 Signaling in Mice. causal interaction,ongoing research,unassigned 4,2,0 3.4.24.86 adam 17 endopeptidase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28947615&form=6&db=m Vascular ADAM17 (a Disintegrin and Metalloproteinase Domain 17) Is Required for Angiotensin II/?-Aminopropionitrile-Induced Abdominal Aortic Aneurysm. causal interaction,therapeutic application,unassigned 4,2,0 3.4.24.86 adam 17 endopeptidase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29632822&form=6&db=m ADAM17 is essential for ectodomain shedding of the EGF-receptor ligand amphiregulin. therapeutic application,unassigned 1,0 3.4.24.86 adam 17 endopeptidase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29930147&form=6&db=m Cell-Specific Functions of ADAM17 Regulate the Progression of Thoracic Aortic Aneurysm. causal interaction,therapeutic application,unassigned 4,1,0 3.4.24.86 adam 17 endopeptidase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30355783&form=6&db=m Structural and Functional Analyses of the Shedding Protease ADAM17 in HoxB8-Immortalized Macrophages and Dendritic-like Cells. causal interaction,unassigned 4,0 3.4.24.86 adam 17 endopeptidase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31257400&form=6&db=m The ADAM17 Protease Promotes Tobacco Smoke Carcinogen-induced Lung Tumourigenesis. causal interaction,ongoing research,therapeutic application,unassigned 3,3,4,0 3.4.24.86 adam 17 endopeptidase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33181031&form=6&db=m ADAM17 Deficiency Protects against Pulmonary Emphysema. causal interaction,ongoing research,therapeutic application,unassigned 4,3,4,0 3.4.24.86 adam 17 endopeptidase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33585287&form=6&db=m The Threshold Effect: Lipopolysaccharide-Induced Inflammatory Responses in Primary Macrophages Are Differentially Regulated in an iRhom2-Dependent Manner. unassigned - 3.4.24.86 adam 17 endopeptidase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34075077&form=6&db=m ADAM10 and ADAM17 regulate EGFR, c-Met and TNF RI signalling in liver regeneration and fibrosis. causal interaction,unassigned 4,0 3.4.24.86 adam10 endopeptidase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18393804&form=6&db=m Part-time alpha-secretases: the functional biology of ADAM 9, 10 and 17. causal interaction,diagnostic usage,unassigned 1,3,0 3.4.24.86 adam10 endopeptidase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20644114&form=6&db=m Differentially regulated GPVI ectodomain shedding by multiple platelet-expressed proteinases. ongoing research,unassigned 4,0 3.4.24.86 adam10 endopeptidase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34075077&form=6&db=m ADAM10 and ADAM17 regulate EGFR, c-Met and TNF RI signalling in liver regeneration and fibrosis. causal interaction,unassigned 4,0 3.4.24.86 Adenocarcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29029414&form=6&db=m Targeting ADAM17 inhibits human colorectal adenocarcinoma progression and tumor-initiating cell frequency. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,1,3,1 3.4.24.86 Adenocarcinoma of Lung http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26111641&form=6&db=m Adam17, a Target of Mir-326, Promotes Emt-Induced Cells Invasion in Lung Adenocarcinoma. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,4,1 3.4.24.86 Adenocarcinoma of Lung http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28960861&form=6&db=m Lentivirus-mediated disintegrin and metalloproteinase 17 RNA interference reversed the acquired resistance to gefitinib in lung adenocarcinoma cells in vitro. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,3,4,3 3.4.24.86 Adenocarcinoma of Lung http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31257400&form=6&db=m The ADAM17 Protease Promotes Tobacco Smoke Carcinogen-induced Lung Tumourigenesis. causal interaction,ongoing research,therapeutic application,unassigned 3,3,4,0 3.4.24.86 Albuminuria http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23646149&form=6&db=m Rosiglitazone treatment of type 2 diabetic db/db mice attenuates urinary albumin and angiotensin converting enzyme 2 excretion. ongoing research,therapeutic application,unassigned 4,1,0 3.4.24.86 Albuminuria http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24756098&form=6&db=m Daily exercise training protects against albuminuria and angiotensin converting enzyme 2 shedding in db/db diabetic mice. causal interaction,ongoing research,therapeutic application,unassigned 2,4,2,0 3.4.24.86 Alzheimer Disease http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11032903&form=6&db=m Coordinated expression of beta-amyloid precursor protein and the putative beta-secretase BACE and alpha-secretase ADAM10 in mouse and human brain. diagnostic usage,ongoing research,unassigned 1,3,0 3.4.24.86 Alzheimer Disease http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19234765&form=6&db=m Reduced neuronal co-localisation of nardilysin and the putative alpha-secretases ADAM10 and ADAM17 in Alzheimer's disease and Down syndrome brains. causal interaction,ongoing research,unassigned 4,1,0 3.4.24.86 Alzheimer Disease http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20184396&form=6&db=m ADAM-17: the enzyme that does it all. causal interaction,therapeutic application,unassigned 4,1,0 3.4.24.86 Alzheimer Disease http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20627730&form=6&db=m The relationship between ADAM17 promoter polymorphisms and sporadic Alzheimer's disease in a Northern Chinese Han population. ongoing research,unassigned 1,0 3.4.24.86 Alzheimer Disease http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21570469&form=6&db=m ERK1-independent ?-secretase cut of ?-amyloid precursor protein via M1 muscarinic receptors and PKC?/?. therapeutic application,unassigned 3,0 3.4.24.86 Alzheimer Disease http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26119306&form=6&db=m The Distinct Role of ADAM17 in APP Proteolysis and Microglial Activation Related to Alzheimer's Disease. causal interaction,unassigned 1,0 3.4.24.86 Alzheimer Disease http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29988083&form=6&db=m A rare loss-of-function variant of ADAM17 is associated with late-onset familial Alzheimer disease. causal interaction,unassigned 4,0 3.4.24.86 Alzheimer Disease http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34537230&form=6&db=m Quercetin stimulates the non-amyloidogenic pathway via activation of ADAM10 and ADAM17 gene expression in aluminum chloride-induced Alzheimer's disease rat model. ongoing research,unassigned 2,0 3.4.24.86 Aneurysm http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21712436&form=6&db=m Transcriptional Profiling and Network Analysis of the Murine Angiotensin II-Induced Abdominal Aortic Aneurysm. causal interaction,unassigned 2,0 3.4.24.86 Aneurysm http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32309850&form=6&db=m Factor XII blockade inhibits aortic dilatation in angiotensin II-infused apolipoprotein E-deficient mice. causal interaction,unassigned 4,0 3.4.24.86 Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25788529&form=6&db=m Circulating ADAM17 Level Reflects Disease Activity in Proteinase-3 ANCA-Associated Vasculitis. causal interaction,diagnostic usage,ongoing research,therapeutic application 2,3,2,1 3.4.24.86 Aortic Aneurysm, Abdominal http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24853957&form=6&db=m Analysis of ADAM17 polymorphisms and susceptibility to sporadic abdominal aortic aneurysm. causal interaction,diagnostic usage,unassigned 4,4,0 3.4.24.86 Aortic Aneurysm, Abdominal http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26422658&form=6&db=m Proteolytically active ADAM10 and ADAM17 carried on membrane microvesicles in human abdominal aortic aneurysms. ongoing research,unassigned 4,0 3.4.24.86 Aortic Aneurysm, Abdominal http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28947615&form=6&db=m Vascular ADAM17 (a Disintegrin and Metalloproteinase Domain 17) Is Required for Angiotensin II/?-Aminopropionitrile-Induced Abdominal Aortic Aneurysm. causal interaction,therapeutic application,unassigned 4,2,0 3.4.24.86 Aortic Aneurysm, Thoracic http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20621845&form=6&db=m Elevation of ADAM10, ADAM17, MMP-2 and MMP-9 expression with media degeneration features CaCl2-induced thoracic aortic aneurysm in a rat model. causal interaction,ongoing research,unassigned 1,3,0 3.4.24.86 Aortic Aneurysm, Thoracic http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29930147&form=6&db=m Cell-Specific Functions of ADAM17 Regulate the Progression of Thoracic Aortic Aneurysm. causal interaction,therapeutic application,unassigned 4,1,0 3.4.24.86 Arthritis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12061836&form=6&db=m Differential effects between marimastat, a TNF-alpha converting enzyme inhibitor, and anti-TNF-alpha antibody on murine models for sepsis and arthritis. ongoing research,therapeutic application,unassigned 4,2,0 3.4.24.86 Arthritis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28815577&form=6&db=m Emerging roles of rhomboid-like pseudoproteases in inflammatory and innate immune responses. causal interaction,unassigned 2,0 3.4.24.86 Arthritis, Rheumatoid http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12670535&form=6&db=m Identification of a selectivity determinant for inhibition of tumor necrosis factor-alpha converting enzyme by comparative modeling. causal interaction,diagnostic usage,therapeutic application,unassigned 3,3,4,0 3.4.24.86 Arthritis, Rheumatoid http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=14579524&form=6&db=m Design strategies for the identification of MMP-13 and Tace inhibitors. causal interaction,therapeutic application,unassigned 4,4,0 3.4.24.86 Arthritis, Rheumatoid http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17332143&form=6&db=m Effect of DPC 333 [(2R)-2-{(3R)-3-amino-3-[4-(2-methylquinolin-4-ylmethoxy)phenyl]-2-oxopyrrolidin-1-yl}-N-hydroxy-4-methylpentanamide], a human tumor necrosis factor alpha-converting enzyme inhibitor, on the disposition of methotrexate: a transporter-based drug-drug interaction case study. causal interaction,ongoing research,therapeutic application,unassigned 2,2,4,0 3.4.24.86 Arthritis, Rheumatoid http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19729328&form=6&db=m Prediction of novel and selective TNF-alpha converting enzyme (TACE) inhibitors and characterization of correlative molecular descriptors by machine learning approaches. causal interaction,therapeutic application,unassigned 4,4,0 3.4.24.86 Arthritis, Rheumatoid http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20184396&form=6&db=m ADAM-17: the enzyme that does it all. causal interaction,therapeutic application,unassigned 4,1,0 3.4.24.86 Arthritis, Rheumatoid http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20871631&form=6&db=m A transforming Src mutant increases the bioavailability of EGFR ligands via stimulation of the cell-surface metalloproteinase ADAM17. causal interaction,ongoing research,therapeutic application,unassigned 3,3,2,0 3.4.24.86 Arthritis, Rheumatoid http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23897050&form=6&db=m Role of ADAM17, p38 MAPK, cathepsins, and proteasome pathway in the synthesis and shedding of fractalkine/CX3CL1 in rheumatoid arthritis. causal interaction,unassigned 2,0 3.4.24.86 Arthritis, Rheumatoid http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24361716&form=6&db=m Glycosylation of a disintegrin and metalloprotease 17 affects its activity and inhibition. unassigned - 3.4.24.86 Arthritis, Rheumatoid http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25013379&form=6&db=m Targeting the sheddase activity of ADAM17 by an anti-ADAM17 antibody D1(A12) inhibits head and neck squamous cell carcinoma cell proliferation and motility via blockage of bradykinin induced HERs transactivation. causal interaction,ongoing research,therapeutic application,unassigned 4,4,4,0 3.4.24.86 Arthritis, Rheumatoid http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25598752&form=6&db=m Reduction of Serum ADAM17 Level Accompanied with Decreased Cytokines after Abatacept Therapy in Patients with Rheumatoid Arthritis. causal interaction,diagnostic usage,therapeutic application,unassigned 4,4,1,0 3.4.24.86 Arthritis, Rheumatoid http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25962601&form=6&db=m Macrophage activity assessed by soluble CD163 in early rheumatoid arthritis: association with disease activity but different response patterns to synthetic and biologic DMARDs. causal interaction,unassigned 4,0 3.4.24.86 Arthritis, Rheumatoid http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27330157&form=6&db=m A disintegrin and metalloprotease-17 and galectin-9 are important regulators of local 4-1BB activity and disease outcome in rheumatoid arthritis. causal interaction,unassigned 3,0 3.4.24.86 Arthritis, Rheumatoid http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30071898&form=6&db=m ADAM-17 is expressed on rheumatoid arthritis fibroblast-like synoviocytes and regulates proinflammatory mediator expression and monocyte adhesion. causal interaction,diagnostic usage,ongoing research,unassigned 2,4,4,0 3.4.24.86 Arthritis, Rheumatoid http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31369701&form=6&db=m Novel functions of inactive rhomboid proteins in immunity and disease. causal interaction,unassigned 3,0 3.4.24.86 Arthritis, Rheumatoid http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32214841&form=6&db=m ADAM17 Genetic Variants and the Response of TNF-? Inhibitor in Rheumatoid Arthritis Patients. ongoing research,therapeutic application,unassigned 1,4,0 3.4.24.86 Asthma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24627531&form=6&db=m Glucocorticoids induce the production of the chemoattractant CCL20 in airway epithelium. causal interaction,unassigned 3,0 3.4.24.86 Asthma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28703301&form=6&db=m The xenoestrogens biphenol-A and nonylphenol differentially regulate metalloprotease-mediated shedding of EGFR ligands. causal interaction,therapeutic application,unassigned 1,4,0 3.4.24.86 Asthma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33455043&form=6&db=m ACE2 expression is elevated in airway epithelial cells from older and male healthy individuals but reduced in asthma. causal interaction,diagnostic usage,unassigned 3,1,0 3.4.24.86 Asthma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34051616&form=6&db=m Abnormal ADAM17 expression causes airway fibrosis in chronic obstructive asthma. causal interaction,unassigned 4,0 3.4.24.86 Astrocytoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24295810&form=6&db=m Carnosic acid suppresses the production of amyloid-? 1-42 and 1-43 by inducing an ?-secretase TACE/ADAM17 in U373MG human astrocytoma cells. ongoing research,unassigned 2,0 3.4.24.86 Atherosclerosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18356551&form=6&db=m Increased ADAM17 mRNA expression and activity is associated with atherosclerosis resistance in LDL-receptor deficient mice. causal interaction,therapeutic application,unassigned 4,1,0 3.4.24.86 Atherosclerosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19154693&form=6&db=m [The two sides of ADAM17 in inflammation: implications in atherosclerosis and obesity] causal interaction,therapeutic application,unassigned 4,1,0 3.4.24.86 Atherosclerosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19253070&form=6&db=m ADAM-9, ADAM-15, and ADAM-17 are upregulated in macrophages in advanced human atherosclerotic plaques in aorta and carotid and femoral arteries--Tampere vascular study. causal interaction,therapeutic application,unassigned 4,1,0 3.4.24.86 Atherosclerosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23384719&form=6&db=m The role of ADAM17 in metabolic inflammation. causal interaction,unassigned 4,0 3.4.24.86 Atherosclerosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24412389&form=6&db=m A disintegrin and metalloproteinase 17 (ADAM17) mediates epidermal growth factor receptor transactivation by angiotensin II on hepatic stellate cells. causal interaction,unassigned 4,0 3.4.24.86 Atherosclerosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24727681&form=6&db=m Association between ADAM17 Promoter Polymorphisms and Ischemic Stroke in a Chinese Population. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,2,3,1 3.4.24.86 Atherosclerosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24813629&form=6&db=m MiR-152 reduces human umbilical vein endothelial cell proliferation and migration by targeting ADAM17. causal interaction,diagnostic usage,unassigned 4,3,0 3.4.24.86 Atherosclerosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24871629&form=6&db=m Vascular Induction of a Disintegrin and Metalloprotease 17 by Angiotensin II Through Hypoxia Inducible Factor 1? causal interaction,therapeutic application,unassigned 3,1,0 3.4.24.86 Atherosclerosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25687272&form=6&db=m A score including ADAM17 substrates correlates to recurring cardiovascular event in subjects with atherosclerosis. causal interaction,unassigned 3,0 3.4.24.86 Atherosclerosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26514426&form=6&db=m Cilostazol inhibits interleukin-1-induced ADAM17 expression through cAMP independent signaling in vascular smooth muscle cells. causal interaction,unassigned 3,0 3.4.24.86 Atherosclerosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26655882&form=6&db=m Gene silencing of TACE enhances plaque stability and improves vascular remodeling in a rabbit model of atherosclerosis. ongoing research,therapeutic application,unassigned 1,1,0 3.4.24.86 Atherosclerosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28004058&form=6&db=m Contrasting effects of myeloid and endothelial ADAM17 on atherosclerosis development. ongoing research,unassigned 4,0 3.4.24.86 Atherosclerosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28062509&form=6&db=m Adam17 Deficiency Promotes Atherosclerosis by Enhanced TNFR2 Signaling in Mice. causal interaction,ongoing research,unassigned 4,2,0 3.4.24.86 Atherosclerosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28122773&form=6&db=m ADAM17: A Molecular Switch to Control TNFR2 During Atherogenesis In Vivo. ongoing research,unassigned 2,0 3.4.24.86 Atherosclerosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29874690&form=6&db=m A Disintegrin and Metalloproteases (ADAMs) in Cardiovascular, Metabolic and Inflammatory Diseases: Aspects for Theranostic Approaches. causal interaction,unassigned 4,0 3.4.24.86 Atherosclerosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31141400&form=6&db=m Role of ADAM17 in kidney disease. causal interaction,ongoing research,therapeutic application,unassigned 4,3,4,0 3.4.24.86 Atherosclerosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33330676&form=6&db=m The Role of iRhom2 in Metabolic and Cardiovascular-Related Disorders. causal interaction,therapeutic application,unassigned 4,1,0 3.4.24.86 Autoimmune Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12670535&form=6&db=m Identification of a selectivity determinant for inhibition of tumor necrosis factor-alpha converting enzyme by comparative modeling. causal interaction,diagnostic usage,therapeutic application,unassigned 3,3,4,0 3.4.24.86 Autoimmune Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25171914&form=6&db=m ADAM17 at the interface between inflammation and autoimmunity. causal interaction,diagnostic usage,therapeutic application,unassigned 4,2,1,0 3.4.24.86 Autoimmune Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25386842&form=6&db=m New Insights Into ADAMs Regulation of the GRO-?/CXCR2 System: Focus on Sjögren's Syndrome. causal interaction,therapeutic application,unassigned 3,4,0 3.4.24.86 Autoimmune Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25962601&form=6&db=m Macrophage activity assessed by soluble CD163 in early rheumatoid arthritis: association with disease activity but different response patterns to synthetic and biologic DMARDs. causal interaction,unassigned 4,0 3.4.24.86 Autoimmune Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31369701&form=6&db=m Novel functions of inactive rhomboid proteins in immunity and disease. causal interaction,unassigned 3,0 3.4.24.86 Autoimmune Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32222277&form=6&db=m Distance dependent shedding of IL-6R. causal interaction,unassigned 3,0 3.4.24.86 Bacteremia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27059842&form=6&db=m Targeting ADAM17 in leukocytes increases neutrophil recruitment and reduces bacterial spread during polymicrobial sepsis. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,2,1 3.4.24.86 Bacterial Infections http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22623356&form=6&db=m ADAM17 activation in circulating neutrophils following bacterial challenge impairs their recruitment. causal interaction,ongoing research,therapeutic application,unassigned 3,2,2,0 3.4.24.86 Brain Injuries http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16790761&form=6&db=m Doxycycline reduces mortality and injury to the brain and cochlea in experimental pneumococcal meningitis. causal interaction,unassigned 4,0 3.4.24.86 Brain Injuries, Traumatic http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30154402&form=6&db=m Specific inhibition of ADAM17/TACE promotes neurogenesis in the injured motor cortex. causal interaction,therapeutic application,unassigned 3,4,0 3.4.24.86 Brain Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17355261&form=6&db=m Inhibition of ADAM17 reduces hypoxia-induced brain tumor cell invasiveness. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,4,4 3.4.24.86 Brain Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19395875&form=6&db=m ADAM17 promotes breast cancer cell malignant phenotype through EGFR-PI3K-AKT activation. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,3,4,1 3.4.24.86 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15492278&form=6&db=m Modulation of gene expression in human central nervous system tumors under methionine deprivation-induced stress. causal interaction,ongoing research,unassigned 1,1,0 3.4.24.86 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15784625&form=6&db=m Nectin-4, a new serological breast cancer marker, is a substrate for tumor necrosis factor-alpha-converting enzyme (TACE)/ADAM-17. causal interaction,therapeutic application,unassigned 2,3,0 3.4.24.86 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17218988&form=6&db=m Targeting TACE-dependent EGFR ligand shedding in breast cancer. causal interaction,unassigned 1,0 3.4.24.86 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17227756&form=6&db=m Post-transcriptional up-regulation of ADAM17 upon epidermal growth factor receptor activation and in breast tumors. causal interaction,diagnostic usage,ongoing research,unassigned 3,2,1,0 3.4.24.86 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17438092&form=6&db=m ADAM-17 expression in breast cancer correlates with variables of tumor progression. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,4,2 3.4.24.86 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18238782&form=6&db=m ADAM-17 predicts adverse outcome in patients with breast cancer. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,4,3 3.4.24.86 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19395875&form=6&db=m ADAM17 promotes breast cancer cell malignant phenotype through EGFR-PI3K-AKT activation. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,3,4,1 3.4.24.86 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21203579&form=6&db=m HER2 phosphorylation is maintained by a PKB negative feedback loop in response to anti-HER2 herceptin in breast cancer. causal interaction,unassigned 2,0 3.4.24.86 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21240579&form=6&db=m ADAM12 and ADAM17 Gene Expression in Laser-capture Microdissected and Non-microdissected Breast Tumors. causal interaction,diagnostic usage,ongoing research,unassigned 4,1,4,0 3.4.24.86 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21480393&form=6&db=m ADAM17 promotes glioma cell malignant phenotype. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,4,1 3.4.24.86 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22509934&form=6&db=m A novel bispecific single-chain antibody for ADAM17 and CD3 induces T-cell-mediated lysis of prostate cancer cells. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,3,4,1 3.4.24.86 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22940887&form=6&db=m ADAM17-overexpressing breast cancer cells selectively targeted by antibody-toxin conjugates. causal interaction,therapeutic application,unassigned 1,3,0 3.4.24.86 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22967992&form=6&db=m ADAM-17: a novel therapeutic target for triple negative breast cancer. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,2,4,4 3.4.24.86 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23684931&form=6&db=m Human breast cancer-associated fibroblasts enhance cancer cell proliferation through increased TGF-? cleavage by ADAM17. causal interaction,ongoing research,therapeutic application,unassigned 4,4,4,0 3.4.24.86 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23810013&form=6&db=m ADAM22 as a prognostic and therapeutic drug target in the treatment of endocrine-resistant breast cancer. causal interaction,unassigned 2,0 3.4.24.86 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24072428&form=6&db=m Tumor necrosis factor-alpha-converting enzyme activities and tumor-associated macrophages in breast cancer. causal interaction,ongoing research,unassigned 2,2,0 3.4.24.86 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24736554&form=6&db=m miR-221/222 control luminal breast cancer tumor progression by regulating different targets. unassigned - 3.4.24.86 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27221510&form=6&db=m ADAM17-siRNA inhibits MCF-7 breast cancer through EGFR-PI3K-AKT activation. causal interaction,ongoing research,therapeutic application,unassigned 1,4,2,0 3.4.24.86 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27573075&form=6&db=m A-Disintegrin and Metalloproteinase (ADAM) 17 Enzymatically Degrades Interferon-gamma. causal interaction,ongoing research,therapeutic application,unassigned 3,3,4,0 3.4.24.86 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27658778&form=6&db=m The role of ADAM17 in tumorigenesis and progression of breast cancer. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,3,4 3.4.24.86 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27920432&form=6&db=m Discovery of an enzyme and substrate selective inhibitor of ADAM10 using an exosite-binding glycosylated substrate. causal interaction,therapeutic application,unassigned 3,4,0 3.4.24.86 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28161636&form=6&db=m Diallyl trisulfide, a chemopreventive agent from Allium vegetables, inhibits alpha-secretases in breast cancer cells. causal interaction,diagnostic usage,ongoing research,unassigned 4,4,4,0 3.4.24.86 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28442704&form=6&db=m Discovery of an enzyme and substrate selective inhibitor of ADAM10 using an exosite-binding glycosylated substrate. causal interaction,therapeutic application,unassigned 3,4,0 3.4.24.86 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28703301&form=6&db=m The xenoestrogens biphenol-A and nonylphenol differentially regulate metalloprotease-mediated shedding of EGFR ligands. causal interaction,therapeutic application,unassigned 1,4,0 3.4.24.86 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28982863&form=6&db=m Effects of ADAM10 and ADAM17 Inhibitors on Natural Killer Cell Expansion and Antibody-dependent Cellular Cytotoxicity Against Breast Cancer Cells diagnostic usage,ongoing research,therapeutic application,unassigned 1,4,4,0 3.4.24.86 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29393483&form=6&db=m Short hairpin RNA-mediated gene silencing of ADAM17 inhibits the growth of breast cancer MCF?7 cells in vitro and in vivo and its mechanism of action. causal interaction,ongoing research,unassigned 4,3,0 3.4.24.86 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30056265&form=6&db=m The soluble nectin-4 ecto-domain promotes breast cancer induced angiogenesis via endothelial Integrin-?4. ongoing research,unassigned 2,0 3.4.24.86 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32927582&form=6&db=m ADAM-17: a novel therapeutic target for triple negative breast cancer. causal interaction,therapeutic application,unassigned 3,4,0 3.4.24.86 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33615189&form=6&db=m Identification of Novel MicroRNAs as Promising Therapeutics for SARS-CoV-2 by Regulating the EGFR-ADAM17 Axis: An In Silico Analysis. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,1,1,2 3.4.24.86 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34208863&form=6&db=m Regulation of Platelet-Derived ADAM17: A Biomarker Approach for Breast Cancer? causal interaction,therapeutic application,unassigned 4,1,0 3.4.24.86 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34281556&form=6&db=m Lentiviral CRISPR-guided RNA library screening identified Adam17 as an upstream negative regulator of Procr in mammary epithelium. ongoing research,unassigned 3,0 3.4.24.86 CADASIL http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27476853&form=6&db=m Mechanistic insights into a TIMP3-sensitive pathway constitutively engaged in the regulation of cerebral hemodynamics. therapeutic application,unassigned 2,0 3.4.24.86 Candidiasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21233274&form=6&db=m IL-1{beta} and ADAM17 are central regulators of {beta}-defensin expression in Candida esophagitis. causal interaction,therapeutic application,unassigned 3,1,0 3.4.24.86 Carcinogenesis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12606576&form=6&db=m TACE is required for the activation of the EGFR by TGF-alpha in tumors. causal interaction,unassigned 1,0 3.4.24.86 Carcinogenesis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16912185&form=6&db=m Multiple Acquired Renal Carcinoma Tumor Capabilities Abolished upon Silencing of ADAM17. causal interaction,ongoing research,unassigned 3,4,0 3.4.24.86 Carcinogenesis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19296470&form=6&db=m MicroRNA-122, a tumor suppressor microRNA that regulates intrahepatic metastasis of hepatocellular carcinoma. causal interaction,diagnostic usage,therapeutic application,unassigned 4,1,3,0 3.4.24.86 Carcinogenesis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19843672&form=6&db=m Sheddase Activity of Tumor Necrosis Factor-{alpha} Converting Enzyme Is Increased and Prognostically Valuable in Head and Neck Cancer. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,2,1 3.4.24.86 Carcinogenesis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20551051&form=6&db=m ADAM17 regulates epidermal growth factor receptor expression through the activation of Notch1 in non-small cell lung cancer. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,3,3 3.4.24.86 Carcinogenesis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20871631&form=6&db=m A transforming Src mutant increases the bioavailability of EGFR ligands via stimulation of the cell-surface metalloproteinase ADAM17. causal interaction,ongoing research,therapeutic application,unassigned 3,3,2,0 3.4.24.86 Carcinogenesis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22139867&form=6&db=m Prognostic value of ADAM17 in human gastric cancer. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,4,3 3.4.24.86 Carcinogenesis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22665490&form=6&db=m The cytosolic domain of protein-tyrosine kinase 7 (PTK7), generated from sequential cleavage by a disintegrin and metalloprotease 17 (ADAM17) and ?-secretase, enhances cell proliferation and migration in colon cancer cells. ongoing research,unassigned 4,0 3.4.24.86 Carcinogenesis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22975374&form=6&db=m EGF Receptor Is Required for KRAS-Induced Pancreatic Tumorigenesis. causal interaction,therapeutic application,unassigned 2,2,0 3.4.24.86 Carcinogenesis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23475633&form=6&db=m ADAM17 is overexpressed in non-small cell lung cancer and its expression correlates with poor patient survival. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,4,3 3.4.24.86 Carcinogenesis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24403253&form=6&db=m ADAM17-mediated CD44 cleavage promotes orasphere formation or stemness and tumorigenesis in HNSCC. causal interaction,diagnostic usage,ongoing research,therapeutic application 1,4,4,1 3.4.24.86 Carcinogenesis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27489286&form=6&db=m ADAM17 is a tumor promoter and therapeutic target in Western diet-associated colon cancer. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,3,4,4 3.4.24.86 Carcinogenesis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27658778&form=6&db=m The role of ADAM17 in tumorigenesis and progression of breast cancer. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,3,4 3.4.24.86 Carcinogenesis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28160627&form=6&db=m Interleukin-11-driven gastric tumourigenesis is independent of trans-signalling. causal interaction,diagnostic usage,unassigned 2,1,0 3.4.24.86 Carcinogenesis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28751722&form=6&db=m Hepatocyte specific TIMP3 expression prevents diet dependent fatty liver disease and hepatocellular carcinoma. causal interaction,therapeutic application,unassigned 4,1,0 3.4.24.86 Carcinogenesis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29472497&form=6&db=m ADAM17 is required for EGF-R-induced intestinal tumors via IL-6 trans-signaling. causal interaction,ongoing research,therapeutic application,unassigned 4,3,4,0 3.4.24.86 Carcinogenesis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31257400&form=6&db=m The ADAM17 Protease Promotes Tobacco Smoke Carcinogen-induced Lung Tumourigenesis. causal interaction,ongoing research,therapeutic application,unassigned 3,3,4,0 3.4.24.86 Carcinogenesis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31455669&form=6&db=m Mutagenesis of the ADAM17-phosphatidylserine-binding motif leads to embryonic lethality in mice. causal interaction,unassigned 3,0 3.4.24.86 Carcinogenesis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33042435&form=6&db=m Tetraspanin CD9 interacts with ?-secretase to enhance its oncogenic function in pancreatic cancer. unassigned - 3.4.24.86 Carcinogenesis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33356812&form=6&db=m Upregulation of polycistronic microRNA-143 and microRNA-145 in colonocytes suppresses colitis and inflammation-associated colon cancer. ongoing research,unassigned 4,0 3.4.24.86 Carcinogenesis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34367416&form=6&db=m ADAM17 and NF-?B p65 form a positive feedback loop that facilitates human esophageal squamous cell carcinoma cell viability. causal interaction,ongoing research,unassigned 2,3,0 3.4.24.86 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16041691&form=6&db=m Up-regulated expression of ADAM17 in human colon carcinoma: co-expression with EGFR in neoplastic and endothelial cells. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,4,1 3.4.24.86 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17180679&form=6&db=m ADAM-17 associated with CD44 cleavage and metastasis in oral squamous cell carcinoma. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,2,4,1 3.4.24.86 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17438092&form=6&db=m ADAM-17 expression in breast cancer correlates with variables of tumor progression. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,4,2 3.4.24.86 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17822026&form=6&db=m [Inhibition of proliferation, adhesion and invasion ability of human lung carcinoma cell A549 by tumor necrosis factor-alpha converting enzyme (TACE)] ongoing research,unassigned 3,0 3.4.24.86 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17999917&form=6&db=m Involvement of NF-kappaB-mediated maturation of ADAM-17 in the invasion of oral squamous cell carcinoma. causal interaction,ongoing research,unassigned 3,3,0 3.4.24.86 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19380613&form=6&db=m Soluble Form of the (Pro)Renin Receptor Generated by Intracellular Cleavage by Furin Is Secreted in Plasma. ongoing research,therapeutic application,unassigned 1,1,0 3.4.24.86 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20300969&form=6&db=m ADAM-17 over-expression in gallbladder carcinoma correlates with poor prognosis of patients. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,4,4,3 3.4.24.86 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23251384&form=6&db=m ADAM17 silencing in mouse colon carcinoma cells: the effect on tumoricidal cytokines and angiogenesis. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,4,3 3.4.24.86 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23441135&form=6&db=m MicroRNA-145 Targets the Metalloprotease ADAM17 and Is Suppressed in Renal Cell Carcinoma Patients. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,1,2,1 3.4.24.86 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23545805&form=6&db=m The disintegrin domain of ADAM17 antagonises fibroblast?carcinoma cell interactions. diagnostic usage,ongoing research,unassigned 2,3,0 3.4.24.86 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24054013&form=6&db=m [Clinicopathological and prognostic significance of the expression of ADAM17 mRNA and protein in esophageal squamous cell carcinoma]. diagnostic usage,ongoing research,unassigned 4,4,0 3.4.24.86 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24495306&form=6&db=m ADAM17 mediates OSCC development in an orthotopic murine model. causal interaction,unassigned 4,0 3.4.24.86 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24793016&form=6&db=m ADAM17 is associated with EMMPRIN and predicts poor prognosis in patients with uterine cervical carcinoma. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,4,3 3.4.24.86 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24996774&form=6&db=m A novel marker ADAM17 for clear cell renal cell carcinomas: Implication for patients' prognosis. diagnostic usage,ongoing research,therapeutic application,unassigned 2,3,3,0 3.4.24.86 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25013379&form=6&db=m Targeting the sheddase activity of ADAM17 by an anti-ADAM17 antibody D1(A12) inhibits head and neck squamous cell carcinoma cell proliferation and motility via blockage of bradykinin induced HERs transactivation. causal interaction,ongoing research,therapeutic application,unassigned 4,4,4,0 3.4.24.86 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25351873&form=6&db=m A disintegrin and metalloproteinase 17 mRNA and protein expression in esophageal squamous cell carcinoma, as well as its clinicopathological factors and prognosis. causal interaction,diagnostic usage,ongoing research,unassigned 3,4,4,0 3.4.24.86 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25966212&form=6&db=m Expression and clinical significance of ADAM17 protein in esophageal squamous cell carcinoma. causal interaction,diagnostic usage,ongoing research,unassigned 1,4,4,0 3.4.24.86 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27576135&form=6&db=m Mass spectrometry-based proteomics revealed Glypican-1 as a novel ADAM17 substrate. causal interaction,ongoing research,therapeutic application,unassigned 4,1,2,0 3.4.24.86 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27774114&form=6&db=m The disintegrin-metalloproteinases ADAM10 and ADAM17 are upregulated in cutaneous squamous cell carcinomas. unassigned - 3.4.24.86 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27779657&form=6&db=m ADAM17 promotes epithelial-mesenchymal transition via TGF-?/Smad pathway in gastric carcinoma cells. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,1,2,4 3.4.24.86 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27878499&form=6&db=m Therapeutic potential of ADAM17 modulation in gastric cancer through regulation of the EGFR and TNF-? signalling pathways. causal interaction,diagnostic usage,ongoing research,unassigned 4,3,4,0 3.4.24.86 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29171106&form=6&db=m Autophagy regulates cisplatin-induced stemness and chemoresistance via the upregulation of CD44, ABCB1 and ADAM17 in oral squamous cell carcinoma. causal interaction,diagnostic usage,unassigned 3,2,0 3.4.24.86 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29180185&form=6&db=m ADAM-17 expression is enhanced by FoxM1 and is a poor prognostic sign in gastric carcinoma. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,3,3 3.4.24.86 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31207072&form=6&db=m MicroRNA-224, negatively regulated by c-jun, inhibits growth and epithelial-to-mesenchymal transition phenotype via targeting ADAM17 in oral squamous cell carcinoma. unassigned - 3.4.24.86 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32889897&form=6&db=m MiR-338-3p inhibits cell migration and invasion in human hypopharyngeal cancer via downregulation of ADAM17. causal interaction,ongoing research,therapeutic application,unassigned 4,3,4,0 3.4.24.86 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34367416&form=6&db=m ADAM17 and NF-?B p65 form a positive feedback loop that facilitates human esophageal squamous cell carcinoma cell viability. causal interaction,ongoing research,unassigned 2,3,0 3.4.24.86 Carcinoma, Hepatocellular http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15309730&form=6&db=m ADAM17 mRNA expression and pathological features of hepatocellular carcinoma. causal interaction,diagnostic usage,ongoing research,unassigned 1,4,4,0 3.4.24.86 Carcinoma, Hepatocellular http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18371937&form=6&db=m Inhibition of the EGF receptor blocks autocrine growth and increases the cytotoxic effects of doxorubicin in rat hepatoma cells: role of reactive oxygen species production and glutathione depletion. diagnostic usage,ongoing research,unassigned 3,3,0 3.4.24.86 Carcinoma, Hepatocellular http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19296470&form=6&db=m MicroRNA-122, a tumor suppressor microRNA that regulates intrahepatic metastasis of hepatocellular carcinoma. causal interaction,diagnostic usage,therapeutic application,unassigned 4,1,3,0 3.4.24.86 Carcinoma, Hepatocellular http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20922190&form=6&db=m Effects of pro-inflammatory cytokines on the production of soluble fractalkine and ADAM17 by HepG2 cells. causal interaction,diagnostic usage,ongoing research,unassigned 3,2,4,0 3.4.24.86 Carcinoma, Hepatocellular http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23621665&form=6&db=m miR-145 suppresses cell invasion in hepatocellular carcinoma cells: miR-145 targets ADAM17. causal interaction,ongoing research,therapeutic application,unassigned 2,3,1,0 3.4.24.86 Carcinoma, Hepatocellular http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23625205&form=6&db=m ADAM17 mediates hypoxia-induced drug resistance in hepatocellular carcinoma cells through activation of EGFR/PI3K/Akt pathway. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,1,4,3 3.4.24.86 Carcinoma, Hepatocellular http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24969373&form=6&db=m Expression of miR-224, miR-145, and their putative target ADAM17 in hepatocellular carcinoma. ongoing research,unassigned 2,0 3.4.24.86 Carcinoma, Hepatocellular http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25174729&form=6&db=m MicroRNA-145 inhibits cell proliferation by directly targeting ADAM17 in hepatocellular carcinoma. therapeutic application,unassigned 1,0 3.4.24.86 Carcinoma, Hepatocellular http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26993601&form=6&db=m Role of ADAM17 in invasion and migration of CD133-expressing liver cancer stem cells after irradiation. causal interaction,diagnostic usage,ongoing research,unassigned 1,3,3,0 3.4.24.86 Carcinoma, Hepatocellular http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29873070&form=6&db=m Enzymatic inhibition of MICA sheddase ADAM17 by lomofungin in hepatocellular carcinoma cells. therapeutic application,unassigned 1,0 3.4.24.86 Carcinoma, Hepatocellular http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29966664&form=6&db=m ADAM17 promotes cell migration and invasion through the integrin ?1 pathway in hepatocellular carcinoma. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,4,4 3.4.24.86 Carcinoma, Hepatocellular http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29970890&form=6&db=m Novel ADAM-17 inhibitor ZLDI-8 enhances the in vitro and in vivo chemotherapeutic effects of Sorafenib on hepatocellular carcinoma cells. ongoing research,therapeutic application,unassigned 3,4,0 3.4.24.86 Carcinoma, Hepatocellular http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31007696&form=6&db=m Inhibition of hepatocellular carcinoma cell proliferation, migration, and invasion by a disintegrin and metalloproteinase-17 inhibitor TNF484. causal interaction,unassigned 3,0 3.4.24.86 Carcinoma, Hepatocellular http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31611551&form=6&db=m MicroRNA-3163 targets ADAM-17 and enhances the sensitivity of hepatocellular carcinoma cells to molecular targeted agents. therapeutic application,unassigned 3,0 3.4.24.86 Carcinoma, Hepatocellular http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31978449&form=6&db=m Novel ADAM-17 inhibitor ZLDI-8 inhibits the metastasis of hepatocellular carcinoma by reversing epithelial-mesenchymal transition in vitro and in vivo. ongoing research,therapeutic application,unassigned 4,3,0 3.4.24.86 Carcinoma, Hepatocellular http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32210451&form=6&db=m HNF-4? inhibits hepatocellular carcinoma cell proliferation through mir-122-adam17 pathway. therapeutic application,unassigned 1,0 3.4.24.86 Carcinoma, Hepatocellular http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32405532&form=6&db=m GPR50 Promotes Hepatocellular Carcinoma Progression via the Notch Signaling Pathway through Direct Interaction with ADAM17. causal interaction,therapeutic application,unassigned 1,1,0 3.4.24.86 Carcinoma, Hepatocellular http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33100908&form=6&db=m ADAM17 promotes the invasion of hepatocellular carcinoma via upregulation MMP21. causal interaction,diagnostic usage,ongoing research,unassigned 4,3,1,0 3.4.24.86 Carcinoma, Non-Small-Cell Lung http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20551051&form=6&db=m ADAM17 regulates epidermal growth factor receptor expression through the activation of Notch1 in non-small cell lung cancer. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,3,3 3.4.24.86 Carcinoma, Non-Small-Cell Lung http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23475633&form=6&db=m ADAM17 is overexpressed in non-small cell lung cancer and its expression correlates with poor patient survival. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,4,3 3.4.24.86 Carcinoma, Non-Small-Cell Lung http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24626788&form=6&db=m ADAM17 silencing suppresses the migration and invasion of non-small cell lung cancer. causal interaction,ongoing research,therapeutic application,unassigned 3,3,1,0 3.4.24.86 Carcinoma, Non-Small-Cell Lung http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25363527&form=6&db=m Estrogen upregulates MICA/B expression in human non-small cell lung cancer through the regulation of ADAM17. ongoing research,therapeutic application,unassigned 2,1,0 3.4.24.86 Carcinoma, Non-Small-Cell Lung http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27076628&form=6&db=m Secretome Signature Identifies ADAM17 as Novel Target for Radiosensitization of Non-Small Cell Lung Cancer. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,3,4,4 3.4.24.86 Carcinoma, Non-Small-Cell Lung http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27618869&form=6&db=m Savior or not: ADAM17 inhibitors overcome radiotherapy-resistance in non-small cell lung cancer. therapeutic application,unassigned 3,0 3.4.24.86 Carcinoma, Renal Cell http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16912185&form=6&db=m Multiple Acquired Renal Carcinoma Tumor Capabilities Abolished upon Silencing of ADAM17. causal interaction,ongoing research,unassigned 3,4,0 3.4.24.86 Carcinoma, Renal Cell http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23441135&form=6&db=m MicroRNA-145 Targets the Metalloprotease ADAM17 and Is Suppressed in Renal Cell Carcinoma Patients. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,1,2,1 3.4.24.86 Carcinoma, Renal Cell http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23659326&form=6&db=m Inhibition of ADAM-17 more effectively down-regulates the Notch pathway than that of ?-secretase in renal carcinoma. causal interaction,therapeutic application,unassigned 4,1,0 3.4.24.86 Carcinoma, Renal Cell http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24996774&form=6&db=m A novel marker ADAM17 for clear cell renal cell carcinomas: Implication for patients' prognosis. diagnostic usage,ongoing research,therapeutic application,unassigned 2,3,3,0 3.4.24.86 Carcinoma, Renal Cell http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29181054&form=6&db=m Predictive values of Notch signalling in renal carcinoma. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,2,1 3.4.24.86 Carcinoma, Squamous Cell http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25013379&form=6&db=m Targeting the sheddase activity of ADAM17 by an anti-ADAM17 antibody D1(A12) inhibits head and neck squamous cell carcinoma cell proliferation and motility via blockage of bradykinin induced HERs transactivation. causal interaction,ongoing research,therapeutic application,unassigned 4,4,4,0 3.4.24.86 Carcinoma, Squamous Cell http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27576135&form=6&db=m Mass spectrometry-based proteomics revealed Glypican-1 as a novel ADAM17 substrate. causal interaction,ongoing research,therapeutic application,unassigned 4,1,2,0 3.4.24.86 Carcinoma, Squamous Cell http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27774114&form=6&db=m The disintegrin-metalloproteinases ADAM10 and ADAM17 are upregulated in cutaneous squamous cell carcinomas. unassigned - 3.4.24.86 Cardiomegaly http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19581512&form=6&db=m Tumor necrosis factor-alpha-converting enzyme is a key regulator of agonist-induced cardiac hypertrophy and fibrosis. causal interaction,diagnostic usage,therapeutic application,unassigned 3,4,2,0 3.4.24.86 Cardiomegaly http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23354118&form=6&db=m Endothelial deletion of ADAM17 in mice results in defective remodeling of the semilunar valves and cardiac dysfunction in adults. causal interaction,therapeutic application,unassigned 1,1,0 3.4.24.86 Cardiomegaly http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23850346&form=6&db=m Upregulation of Nox4 Promotes Angiotensin II-Induced Epidermal Growth Factor Receptor Activation and Subsequent Cardiac Hypertrophy by Increasing ADAM17 Expression. causal interaction,ongoing research,therapeutic application,unassigned 4,2,1,0 3.4.24.86 Cardiomegaly http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24412389&form=6&db=m A disintegrin and metalloproteinase 17 (ADAM17) mediates epidermal growth factor receptor transactivation by angiotensin II on hepatic stellate cells. causal interaction,unassigned 4,0 3.4.24.86 Cardiomegaly http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27480838&form=6&db=m Deleting Vascular ADAM17 Sheds New Light on Hypertensive Cardiac Hypertrophy. unassigned - 3.4.24.86 Cardiomegaly http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30105051&form=6&db=m A Reduction in ADAM17 Expression Is Involved in the Protective Effect of the PPAR-? Activator Fenofibrate on Pressure Overload-Induced Cardiac Hypertrophy. ongoing research,therapeutic application,unassigned 3,4,0 3.4.24.86 Cardiomegaly http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30953402&form=6&db=m Rutaecarpine prevents hypertensive cardiac hypertrophy involving the inhibition of Nox4-ROS-ADAM17 pathway. causal interaction,diagnostic usage,therapeutic application,unassigned 3,3,2,0 3.4.24.86 Cardiomegaly http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34370360&form=6&db=m MiR-26a-5p alleviates cardiac hypertrophy and dysfunction via targeting ADAM17. ongoing research,therapeutic application,unassigned 2,3,0 3.4.24.86 Cardiomyopathies http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16401770&form=6&db=m Altered expression of disintegrin metalloproteinases and their inhibitor in human dilated cardiomyopathy. causal interaction,ongoing research,unassigned 3,4,0 3.4.24.86 Cardiomyopathies http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26136458&form=6&db=m Cardiomyocyte A Disintegrin And Metalloproteinase 17 (ADAM17) Is Essential in Post-Myocardial Infarction Repair by Regulating Angiogenesis. causal interaction,ongoing research,unassigned 2,4,0 3.4.24.86 Cardiomyopathies http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27550917&form=6&db=m A Disintegrin and Metalloprotease-17 Regulates Pressure Overload-Induced Myocardial Hypertrophy and Dysfunction Through Proteolytic Processing of Integrin ?1. causal interaction,therapeutic application,unassigned 4,3,0 3.4.24.86 Cardiomyopathies http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32564294&form=6&db=m Alterations of the renin angiotensin system in human end-stage heart failure before and after mechanical cardiac unloading by LVAD support. diagnostic usage,ongoing research,therapeutic application,unassigned 1,4,2,0 3.4.24.86 Cardiomyopathy, Dilated http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10385500&form=6&db=m Tumor necrosis factor-alpha-converting enzyme and tumor necrosis factor-alpha in human dilated cardiomyopathy. ongoing research,unassigned 4,0 3.4.24.86 Cardiomyopathy, Dilated http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16401770&form=6&db=m Altered expression of disintegrin metalloproteinases and their inhibitor in human dilated cardiomyopathy. causal interaction,ongoing research,unassigned 3,4,0 3.4.24.86 Cardiomyopathy, Dilated http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27550917&form=6&db=m A Disintegrin and Metalloprotease-17 Regulates Pressure Overload-Induced Myocardial Hypertrophy and Dysfunction Through Proteolytic Processing of Integrin ?1. causal interaction,therapeutic application,unassigned 4,3,0 3.4.24.86 Cardiomyopathy, Dilated http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32564294&form=6&db=m Alterations of the renin angiotensin system in human end-stage heart failure before and after mechanical cardiac unloading by LVAD support. diagnostic usage,ongoing research,therapeutic application,unassigned 1,4,2,0 3.4.24.86 Cardiomyopathy, Hypertrophic http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16401770&form=6&db=m Altered expression of disintegrin metalloproteinases and their inhibitor in human dilated cardiomyopathy. causal interaction,ongoing research,unassigned 3,4,0 3.4.24.86 Cardiomyopathy, Hypertrophic http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27550917&form=6&db=m A Disintegrin and Metalloprotease-17 Regulates Pressure Overload-Induced Myocardial Hypertrophy and Dysfunction Through Proteolytic Processing of Integrin ?1. causal interaction,therapeutic application,unassigned 4,3,0 3.4.24.86 Cardiovascular Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24871629&form=6&db=m Vascular Induction of a Disintegrin and Metalloprotease 17 by Angiotensin II Through Hypoxia Inducible Factor 1? causal interaction,therapeutic application,unassigned 3,1,0 3.4.24.86 Cardiovascular Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26514426&form=6&db=m Cilostazol inhibits interleukin-1-induced ADAM17 expression through cAMP independent signaling in vascular smooth muscle cells. causal interaction,unassigned 3,0 3.4.24.86 Cardiovascular Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31141400&form=6&db=m Role of ADAM17 in kidney disease. causal interaction,ongoing research,therapeutic application,unassigned 4,3,4,0 3.4.24.86 Cardiovascular Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33575814&form=6&db=m Contribution of ADAM17 and related ADAMs in cardiovascular diseases. causal interaction,diagnostic usage,unassigned 1,3,0 3.4.24.86 Cholestasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24172289&form=6&db=m Liver protective effect of ursodeoxycholic acid includes regulation of ADAM17 activity. ongoing research,unassigned 2,0 3.4.24.86 Chorioamnionitis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16376986&form=6&db=m Tumour necrosis factor-alpha converting enzyme in human gestational tissues from pregnancies complicated by chorioamnionitis. causal interaction,ongoing research,unassigned 3,2,0 3.4.24.86 Chronic Kidney Disease-Mineral and Bone Disorder http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29056164&form=6&db=m ADAM17, a New Player in the Pathogenesis of Chronic Kidney Disease-Mineral and Bone Disorder. causal interaction,diagnostic usage,ongoing research,unassigned 4,2,2,0 3.4.24.86 Classical Swine Fever http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33684175&form=6&db=m ADAM17 is an essential attachment factor for classical swine fever virus. causal interaction,ongoing research,unassigned 3,1,0 3.4.24.86 Coinfection http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23688779&form=6&db=m ADAM17 silencing by adenovirus encoding miRNA-embedded siRNA revealed essential signal transduction by angiotensin II in vascular smooth muscle cells. ongoing research,therapeutic application,unassigned 1,1,0 3.4.24.86 Colitis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11884025&form=6&db=m Implication of TNF-alpha convertase (TACE/ADAM17) in inducible nitric oxide synthase expression and inflammation in an experimental model of colitis. causal interaction,ongoing research,therapeutic application,unassigned 4,2,2,0 3.4.24.86 Colitis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21041656&form=6&db=m MyD88 signaling in nonhematopoietic cells protects mice against induced colitis by regulating specific EGF receptor ligands. causal interaction,ongoing research,therapeutic application,unassigned 3,3,1,0 3.4.24.86 Colitis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23757215&form=6&db=m TNF? cleavage beyond TACE/ADAM17: matrix metalloproteinase 13 is a potential therapeutic target in sepsis and colitis. causal interaction,therapeutic application,unassigned 2,4,0 3.4.24.86 Colitis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27077118&form=6&db=m Epithelial Cell-Derived a Disintegrin and Metalloproteinase-17 Confers Resistance to Colonic Inflammation Through EGFR Activation. causal interaction,ongoing research,therapeutic application,unassigned 4,4,2,0 3.4.24.86 Colitis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29560122&form=6&db=m The enhanced susceptibility of ADAM-17 hypomorphic mice to DSS-induced colitis is not ameliorated by loss of RIPK3, revealing an unexpected function of ADAM-17 in necroptosis. unassigned - 3.4.24.86 Colitis, Ischemic http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16273118&form=6&db=m Human colonic myocytes are involved in postischemic inflammation through ADAM17-dependent TNFalpha production. ongoing research,therapeutic application,unassigned 1,1,0 3.4.24.86 Colitis, Ulcerative http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19376560&form=6&db=m In situ evidence of involvement of Schwann cells in ulcerative colitis: autocrine and paracrine signaling by A disintegrin and metalloprotease-17-mediated tumor necrosis factor alpha production. causal interaction,diagnostic usage,ongoing research,unassigned 4,3,4,0 3.4.24.86 Colonic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22665490&form=6&db=m The cytosolic domain of protein-tyrosine kinase 7 (PTK7), generated from sequential cleavage by a disintegrin and metalloprotease 17 (ADAM17) and ?-secretase, enhances cell proliferation and migration in colon cancer cells. ongoing research,unassigned 4,0 3.4.24.86 Colonic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27489286&form=6&db=m ADAM17 is a tumor promoter and therapeutic target in Western diet-associated colon cancer. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,3,4,4 3.4.24.86 Colonic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27874952&form=6&db=m Nox1 promotes colon cancer cell metastasis via activation of the ADAM17 pathway. causal interaction,diagnostic usage,ongoing research,unassigned 3,3,1,0 3.4.24.86 Colonic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28349819&form=6&db=m ADAM-17/FHL2 colocalisation suggests interaction and role of these proteins in colorectal cancer. ongoing research,unassigned 4,0 3.4.24.86 Colonic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31060243&form=6&db=m Functional Characterization of Colon Cancer-Associated Mutations in ADAM17: Modifications in the Pro-Domain Interfere with Trafficking and Maturation. causal interaction,ongoing research,unassigned 2,3,0 3.4.24.86 Colonic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31694340&form=6&db=m ADAM17 Activity and IL-6 Trans-Signaling in Inflammation and Cancer. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,4,4 3.4.24.86 Colonic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32450419&form=6&db=m HPP1 Ectodomain Shedding is Mediated by ADAM17 and is Necessary for Tumor Suppression in Colon Cancer. causal interaction,unassigned 3,0 3.4.24.86 Colonic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33356812&form=6&db=m Upregulation of polycistronic microRNA-143 and microRNA-145 in colonocytes suppresses colitis and inflammation-associated colon cancer. ongoing research,unassigned 4,0 3.4.24.86 Colorectal Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20570921&form=6&db=m Chemotherapy-induced activation of ADAM-17: a novel mechanism of drug resistance in colorectal cancer. causal interaction,therapeutic application,unassigned 4,4,0 3.4.24.86 Colorectal Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22677042&form=6&db=m MiR-222 modulates multidrug resistance in human colorectal carcinoma by down-regulating ADAM-17. causal interaction,ongoing research,therapeutic application,unassigned 4,3,4,0 3.4.24.86 Colorectal Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27110571&form=6&db=m Expression of Migration-Related Genes in Human Colorectal Cancer and Activity of a Disintegrin and Metalloproteinase 17. causal interaction,diagnostic usage,ongoing research,unassigned 1,4,4,0 3.4.24.86 Colorectal Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27874952&form=6&db=m Nox1 promotes colon cancer cell metastasis via activation of the ADAM17 pathway. causal interaction,diagnostic usage,ongoing research,unassigned 3,3,1,0 3.4.24.86 Colorectal Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29029414&form=6&db=m Targeting ADAM17 inhibits human colorectal adenocarcinoma progression and tumor-initiating cell frequency. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,1,3,1 3.4.24.86 Colorectal Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29254295&form=6&db=m Serum levels of ADAM10, ADAM12, ADAM17 AND ADAM28 in colorectal cancer patients. diagnostic usage,unassigned 4,0 3.4.24.86 Colorectal Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29964008&form=6&db=m Knockdown of ADAM17 inhibits cell proliferation and increases oxaliplatin sensitivity in HCT-8 colorectal cancer through EGFR-PI3K-AKT activation. ongoing research,therapeutic application,unassigned 3,1,0 3.4.24.86 Colorectal Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30069943&form=6&db=m A novel inhibitor of ADAM17 sensitizes colorectal cancer cells to 5-Fluorouracil by reversing Notch and epithelial-mesenchymal transition in vitro and in vivo. therapeutic application,unassigned 2,0 3.4.24.86 Colorectal Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30514687&form=6&db=m [ADAM17 knockdown increases sensitivity of SW480 cells to cetuximad]. causal interaction,diagnostic usage,ongoing research,unassigned 3,3,4,0 3.4.24.86 Colorectal Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30909692&form=6&db=m Relation between Tetraspanin- Associated and Tetraspanin- Non- Associated Exosomal Proteases and Metabolic Syndrome in Colorectal Cancer Patients diagnostic usage,ongoing research,therapeutic application,unassigned 3,4,1,0 3.4.24.86 Colorectal Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32450419&form=6&db=m HPP1 Ectodomain Shedding is Mediated by ADAM17 and is Necessary for Tumor Suppression in Colon Cancer. causal interaction,unassigned 3,0 3.4.24.86 Communicable Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27784899&form=6&db=m Plasma Ang2 and ADAM17 levels are elevated during clinical malaria; Ang2 level correlates with severity and expression of EPCR-binding PfEMP1. causal interaction,diagnostic usage,ongoing research,unassigned 4,2,3,0 3.4.24.86 Connective Tissue Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31469350&form=6&db=m Association of ADAM17 Expression Levels in Patients with Interstitial Lung Disease. causal interaction,diagnostic usage,ongoing research,unassigned 4,4,4,0 3.4.24.86 Corneal Injuries http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27058125&form=6&db=m ADAM17 Inhibitors Attenuate Corneal Epithelial Detachment Induced by Mustard Exposure. unassigned - 3.4.24.86 Coronavirus Infections http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34416436&form=6&db=m A model for COVID-19-induced dysregulation of ACE2 shedding by ADAM17. unassigned - 3.4.24.86 COVID-19 http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32291449&form=6&db=m ADAM17 inhibition may exert a protective effect on COVID-19. causal interaction,therapeutic application,unassigned 2,4,0 3.4.24.86 COVID-19 http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32769398&form=6&db=m Shedding Light on COVID-19: ADAM17 the Missing Link? causal interaction,diagnostic usage,ongoing research,therapeutic application 3,1,1,4 3.4.24.86 COVID-19 http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32844538&form=6&db=m Alpha-1-antitrypsin: A possible host protective factor against Covid-19. causal interaction,ongoing research,therapeutic application,unassigned 2,1,1,0 3.4.24.86 COVID-19 http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32867008&form=6&db=m Potential interactions of SARS-CoV-2 with human cell receptors in the skin: understanding the enigma for a lower frequency of skin lesions compared to other tissues. unassigned - 3.4.24.86 COVID-19 http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33117379&form=6&db=m ACE2/ADAM17/TMPRSS2 Interplay May Be the Main Risk Factor for COVID-19. diagnostic usage,ongoing research,unassigned 1,2,0 3.4.24.86 COVID-19 http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33239231&form=6&db=m Hypothesis: Alpha-1-antitrypsin is a promising treatment option for COVID-19. causal interaction,ongoing research,therapeutic application,unassigned 3,1,2,0 3.4.24.86 COVID-19 http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33243086&form=6&db=m Assessing COVID-19 susceptibility through analysis of the genetic and epigenetic diversity of ACE2-mediated SARS-CoV-2 entry. causal interaction,diagnostic usage,therapeutic application,unassigned 2,2,3,0 3.4.24.86 COVID-19 http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33243116&form=6&db=m Can Host Cell Proteins Like ACE2, ADAM17, TMPRSS2, Androgen Receptor be the Efficient Targets in SARS-CoV-2 Infection? causal interaction,ongoing research,unassigned 4,4,0 3.4.24.86 COVID-19 http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33275517&form=6&db=m Sex differences in COVID-19: candidate pathways, genetics of ACE2, and sex hormones. causal interaction,unassigned 3,0 3.4.24.86 COVID-19 http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33531686&form=6&db=m More light on cancer and COVID-19 reciprocal interaction. unassigned - 3.4.24.86 COVID-19 http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33615189&form=6&db=m Identification of Novel MicroRNAs as Promising Therapeutics for SARS-CoV-2 by Regulating the EGFR-ADAM17 Axis: An In Silico Analysis. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,1,1,2 3.4.24.86 COVID-19 http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33660945&form=6&db=m Pulmonary, cardiac and renal distribution of ACE2, furin, TMPRSS2 and ADAM17 in rats with heart failure: Potential implication for COVID-19 disease. causal interaction,diagnostic usage,ongoing research,unassigned 3,3,4,0 3.4.24.86 COVID-19 http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33673459&form=6&db=m Upregulation of the Renin-Angiotensin System Pathways and SARS-CoV-2 Infection: The Rationale for the Administration of Zinc-Chelating Agents in COVID-19 Patients. therapeutic application,unassigned 2,0 3.4.24.86 COVID-19 http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34095559&form=6&db=m Ephrin-A1 and the sheddase ADAM12 are upregulated in COVID-19. causal interaction,diagnostic usage,therapeutic application,unassigned 2,2,3,0 3.4.24.86 COVID-19 http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34410424&form=6&db=m Instigators of COVID-19 in Immune Cells are Increased in Tobacco Cigarette Smokers and Electronic Cigarette Vapers Compared to Non-smokers. causal interaction,ongoing research,unassigned 1,2,0 3.4.24.86 COVID-19 http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34419773&form=6&db=m Which ones, when and why should renin-angiotensin system inhibitors work against COVID-19? causal interaction,unassigned 3,0 3.4.24.86 COVID-19 http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34445140&form=6&db=m Severe COVID-19 Patients Show an Increase in Soluble TNFR1 and ADAM17, with a Relationship to Mortality. diagnostic usage,ongoing research,therapeutic application,unassigned 4,3,1,0 3.4.24.86 Crohn Disease http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18493210&form=6&db=m Polymorphisms in the tumor necrosis factor/lipopolysaccharides pathway in Crohn disease in the Jewish Ashkenazi population. ongoing research,unassigned 1,0 3.4.24.86 Crohn Disease http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19299578&form=6&db=m Differential expression and regulation of ADAM17 and TIMP3 in acute inflamed intestinal epithelia. ongoing research,unassigned 3,0 3.4.24.86 Crohn Disease http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19729328&form=6&db=m Prediction of novel and selective TNF-alpha converting enzyme (TACE) inhibitors and characterization of correlative molecular descriptors by machine learning approaches. causal interaction,therapeutic application,unassigned 4,4,0 3.4.24.86 Demyelinating Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16221290&form=6&db=m Tumor necrosis factor-alpha-converting enzyme is expressed in the inflamed peripheral nervous system. causal interaction,unassigned 4,0 3.4.24.86 Demyelinating Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26338334&form=6&db=m Oligodendrocyte Regeneration and CNS Remyelination Require TACE/ADAM17. unassigned - 3.4.24.86 Dermatitis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22565824&form=6&db=m Epidermal ADAM17 maintains the skin barrier by regulating EGFR ligand-dependent terminal keratinocyte differentiation. causal interaction,ongoing research,therapeutic application,unassigned 2,3,1,0 3.4.24.86 Dermatitis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22713436&form=6&db=m Does Adam17 cause the destruction of anchoring fibers via shedding tumor necrosis factor ? in bullous pemphigoid and dermatitis herpetiformis? unassigned - 3.4.24.86 Dermatitis, Atopic http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22284418&form=6&db=m Notch activation by the metalloproteinase ADAM17 regulates myeloproliferation and atopic barrier immunity by suppressing epithelial cytokine synthesis. therapeutic application,unassigned 1,0 3.4.24.86 Dermatomyositis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17207628&form=6&db=m The cell-specific expression of metalloproteinase-disintegrins (ADAMs) in inflammatory myopathies. diagnostic usage,ongoing research,therapeutic application,unassigned 3,4,2,0 3.4.24.86 Dermatomyositis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29411180&form=6&db=m ADAM-17 is expressed in the inflammatory myopathy and is involved with interstitial lung disease. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,4,4 3.4.24.86 Diabetes Mellitus http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34073747&form=6&db=m Both Specific Endothelial and Proximal Tubular Adam17 Deletion Protect against Diabetic Nephropathy. ongoing research,therapeutic application,unassigned 4,1,0 3.4.24.86 Diabetes Mellitus, Type 1 http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26697977&form=6&db=m Paricalcitol modulates ACE2 shedding and renal ADAM17 in NOD mice beyond proteinuria. ongoing research,unassigned 3,0 3.4.24.86 Diabetes Mellitus, Type 1 http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34073747&form=6&db=m Both Specific Endothelial and Proximal Tubular Adam17 Deletion Protect against Diabetic Nephropathy. ongoing research,therapeutic application,unassigned 4,1,0 3.4.24.86 Diabetes Mellitus, Type 2 http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19581416&form=6&db=m TIMP3 is reduced in atherosclerotic plaques from subjects with type 2 diabetes and increased by SirT1. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,3,4,3 3.4.24.86 Diabetes Mellitus, Type 2 http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19633828&form=6&db=m Impaired regulation of the TNF-alpha converting enzyme/tissue inhibitor of metalloproteinase 3 proteolytic system in skeletal muscle of obese type 2 diabetic patients: a new mechanism of insulin resistance in humans. causal interaction,ongoing research,therapeutic application,unassigned 3,4,2,0 3.4.24.86 Diabetes Mellitus, Type 2 http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21406565&form=6&db=m Plasminogen activator inhibitor 1 is an intracellular inhibitor of furin proprotein convertase. causal interaction,diagnostic usage,unassigned 3,3,0 3.4.24.86 Diabetes Mellitus, Type 2 http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29561187&form=6&db=m Increased Urinary Angiotensin Converting Enzyme 2 (ACE2) and Neprilysin (NEP) in Type 2 Diabetic Patients. causal interaction,diagnostic usage,therapeutic application,unassigned 4,3,1,0 3.4.24.86 Diabetes Mellitus, Type 2 http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33904577&form=6&db=m Implications of ADAM17 activation for hyperglycaemia, obesity and type 2 diabetes. causal interaction,ongoing research,therapeutic application,unassigned 3,2,4,0 3.4.24.86 Diabetic Nephropathies http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20566668&form=6&db=m Bradykinin decreases podocyte permeability through ADAM17-dependent epidermal growth factor receptor activation and zonula occludens-1 rearrangement. causal interaction,therapeutic application,unassigned 4,4,0 3.4.24.86 Diabetic Nephropathies http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21289053&form=6&db=m HB-EGF release mediates glucose-induced activation of the epidermal growth factor receptor in mesangial cells. causal interaction,therapeutic application,unassigned 4,4,0 3.4.24.86 Diabetic Nephropathies http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23401241&form=6&db=m Loss of TIMP3 underlies diabetic nephropathy via FoxO1/STAT1 interplay. causal interaction,therapeutic application,unassigned 4,2,0 3.4.24.86 Diabetic Nephropathies http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24756098&form=6&db=m Daily exercise training protects against albuminuria and angiotensin converting enzyme 2 shedding in db/db diabetic mice. causal interaction,ongoing research,therapeutic application,unassigned 2,4,2,0 3.4.24.86 Diabetic Nephropathies http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26175156&form=6&db=m High Glucose Up-regulates ADAM17 through HIF-1? in Mesangial Cells. causal interaction,therapeutic application,unassigned 4,4,0 3.4.24.86 Diabetic Nephropathies http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29361535&form=6&db=m Regulation of profibrotic responses by ADAM17 activation in high glucose requires its C-terminus and FAK. therapeutic application,unassigned 4,0 3.4.24.86 Diabetic Nephropathies http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34073747&form=6&db=m Both Specific Endothelial and Proximal Tubular Adam17 Deletion Protect against Diabetic Nephropathy. ongoing research,therapeutic application,unassigned 4,1,0 3.4.24.86 Diabetic Retinopathy http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32024241&form=6&db=m Role of Endothelial ADAM17 in Early Vascular Changes Associated with Diabetic Retinopathy. causal interaction,unassigned 4,0 3.4.24.86 Diabetic Retinopathy http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33552057&form=6&db=m Evaluation of Proteoforms of the Transmembrane Chemokines CXCL16 and CX3CL1, Their Receptors, and Their Processing Metalloproteinases ADAM10 and ADAM17 in Proliferative Diabetic Retinopathy. ongoing research,unassigned 3,0 3.4.24.86 Down Syndrome http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19234765&form=6&db=m Reduced neuronal co-localisation of nardilysin and the putative alpha-secretases ADAM10 and ADAM17 in Alzheimer's disease and Down syndrome brains. causal interaction,ongoing research,unassigned 4,1,0 3.4.24.86 Encephalomyelitis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15878627&form=6&db=m ADAM-17 and TIMP3 protein and mRNA expression in spinal cord white matter of rats with acute experimental autoimmune encephalomyelitis. ongoing research,unassigned 3,0 3.4.24.86 Encephalomyelitis, Autoimmune, Experimental http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15878627&form=6&db=m ADAM-17 and TIMP3 protein and mRNA expression in spinal cord white matter of rats with acute experimental autoimmune encephalomyelitis. ongoing research,unassigned 3,0 3.4.24.86 Endocrine Gland Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18426733&form=6&db=m Expression of tumor necrosis factor alpha converting enzyme in endocrine cancers. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,3,2,1 3.4.24.86 Endotoxemia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21828049&form=6&db=m Shedding of the MER tyrosine kinase receptor is mediated by ADAM17 through a pathway involving reactive oxygen species, protein kinase {delta}, and P38 map kinase. ongoing research,unassigned 2,0 3.4.24.86 Endotoxemia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26561568&form=6&db=m ADAM17 controls IL-6 signaling by cleavage of the murine IL-6R? from the cell surface of leukocytes during inflammatory responses. unassigned - 3.4.24.86 Endotoxemia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28849138&form=6&db=m Construction of a lentiviral vector containing shRNA targeting ADAM17 and its role in attenuating endotoxemia in mice. ongoing research,therapeutic application,unassigned 4,2,0 3.4.24.86 Endotoxemia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29901075&form=6&db=m [Corrigendum] Construction of a lentiviral vector containing shRNA targeting ADAM17 and its role in attenuating endotoxemia in mice. ongoing research,therapeutic application,unassigned 2,2,0 3.4.24.86 Epiretinal Membrane http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33552057&form=6&db=m Evaluation of Proteoforms of the Transmembrane Chemokines CXCL16 and CX3CL1, Their Receptors, and Their Processing Metalloproteinases ADAM10 and ADAM17 in Proliferative Diabetic Retinopathy. ongoing research,unassigned 3,0 3.4.24.86 Esophageal Squamous Cell Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24054013&form=6&db=m [Clinicopathological and prognostic significance of the expression of ADAM17 mRNA and protein in esophageal squamous cell carcinoma]. diagnostic usage,ongoing research,unassigned 4,4,0 3.4.24.86 Esophageal Squamous Cell Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25351873&form=6&db=m A disintegrin and metalloproteinase 17 mRNA and protein expression in esophageal squamous cell carcinoma, as well as its clinicopathological factors and prognosis. causal interaction,diagnostic usage,ongoing research,unassigned 3,4,4,0 3.4.24.86 Esophageal Squamous Cell Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25966212&form=6&db=m Expression and clinical significance of ADAM17 protein in esophageal squamous cell carcinoma. causal interaction,diagnostic usage,ongoing research,unassigned 1,4,4,0 3.4.24.86 Esophageal Squamous Cell Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34367416&form=6&db=m ADAM17 and NF-?B p65 form a positive feedback loop that facilitates human esophageal squamous cell carcinoma cell viability. causal interaction,ongoing research,unassigned 2,3,0 3.4.24.86 Esophagitis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21233274&form=6&db=m IL-1{beta} and ADAM17 are central regulators of {beta}-defensin expression in Candida esophagitis. causal interaction,therapeutic application,unassigned 3,1,0 3.4.24.86 Fatty Liver http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28751722&form=6&db=m Hepatocyte specific TIMP3 expression prevents diet dependent fatty liver disease and hepatocellular carcinoma. causal interaction,therapeutic application,unassigned 4,1,0 3.4.24.86 Fibrosarcoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26535007&form=6&db=m Deletions in the cytoplasmic domain of iRhom1 and iRhom2 promote shedding of the TNF receptor by the protease ADAM17. causal interaction,ongoing research,unassigned 2,3,0 3.4.24.86 Gastrointestinal Stromal Tumors http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19298600&form=6&db=m Up-regulated expression of ADAM17 in gastrointestinal stromal tumors: coexpression with EGFR and EGFR ligands. causal interaction,diagnostic usage,ongoing research,unassigned 4,3,1,0 3.4.24.86 Glioblastoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19657395&form=6&db=m Gene expression analysis of an EGFR indirectly related pathway identified PTEN and MMP9 as reliable diagnostic markers for human glial tumor specimens. diagnostic usage,unassigned 4,0 3.4.24.86 Glioblastoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23356982&form=6&db=m ADAM17 regulates self-renewal and differentiation of U87 glioblastoma stem cells. ongoing research,unassigned 3,0 3.4.24.86 Glioblastoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23470260&form=6&db=m ADAM17 promotes U87 glioblastoma stem cell migration and invasion. causal interaction,diagnostic usage,therapeutic application,unassigned 4,3,4,0 3.4.24.86 Glioblastoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27540907&form=6&db=m PDIA6 regulation of ADAM17 shedding activity and EGFR-mediated migration and invasion of glioblastoma cells. causal interaction,ongoing research,unassigned 4,4,0 3.4.24.86 Glioblastoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27541285&form=6&db=m Metalloproteinases ADAM10 and ADAM17 Mediate Migration and Differentiation in Glioblastoma Sphere-Forming Cells. causal interaction,ongoing research,therapeutic application,unassigned 3,3,4,0 3.4.24.86 Glioma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17355261&form=6&db=m Inhibition of ADAM17 reduces hypoxia-induced brain tumor cell invasiveness. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,4,4 3.4.24.86 Glioma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18358600&form=6&db=m Sensitization of cerebral tissue in nude mice with photodynamic therapy induces ADAM17/TACE and promotes glioma cell invasion. unassigned - 3.4.24.86 Glioma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19395875&form=6&db=m ADAM17 promotes breast cancer cell malignant phenotype through EGFR-PI3K-AKT activation. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,3,4,1 3.4.24.86 Glioma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19772640&form=6&db=m Transcription factor Sp1 induces ADAM17 and contributes to tumor cell invasiveness under hypoxia. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,3,4,1 3.4.24.86 Glioma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21359495&form=6&db=m TGF-?1 promotes motility and invasiveness of glioma cells through activation of ADAM17. causal interaction,unassigned 2,0 3.4.24.86 Glioma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21480393&form=6&db=m ADAM17 promotes glioma cell malignant phenotype. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,4,1 3.4.24.86 Glioma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23076445&form=6&db=m MiR-145 reduces ADAM17 expression and inhibits in vitro migration and invasion of glioma cells. causal interaction,ongoing research,unassigned 1,4,0 3.4.24.86 Glioma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23356982&form=6&db=m ADAM17 regulates self-renewal and differentiation of U87 glioblastoma stem cells. ongoing research,unassigned 3,0 3.4.24.86 Glioma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23470260&form=6&db=m ADAM17 promotes U87 glioblastoma stem cell migration and invasion. causal interaction,diagnostic usage,therapeutic application,unassigned 4,3,4,0 3.4.24.86 Glioma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24185966&form=6&db=m Effects of tetrandrine on glioma cell malignant phenotype via inhibition of ADAM17. causal interaction,diagnostic usage,ongoing research,unassigned 4,4,4,0 3.4.24.86 Glioma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25301262&form=6&db=m Dihydroartemisinin suppresses glioma proliferation and invasion via inhibition of the ADAM17 pathway. causal interaction,therapeutic application,unassigned 4,1,0 3.4.24.86 Glioma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25364437&form=6&db=m Diagnostic and prognostic value of a disintegrin and metalloproteinase-17 in patients with gliomas. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,4,4 3.4.24.86 Glioma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25544346&form=6&db=m Overexpression of miR?145 in U87 cells reduces glioma cell malignant phenotype and promotes survival after in vivo implantation. causal interaction,unassigned 1,0 3.4.24.86 Glioma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29131255&form=6&db=m The correlation between the expression of ADAM17, EGFR and Ki-67 in malignant gliomas. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,2,2 3.4.24.86 Glioma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29700308&form=6&db=m FoxM1 drives ADAM17/EGFR activation loop to promote mesenchymal transition in glioblastoma. causal interaction,unassigned 1,0 3.4.24.86 Gliosarcoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17355261&form=6&db=m Inhibition of ADAM17 reduces hypoxia-induced brain tumor cell invasiveness. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,4,4 3.4.24.86 Glomerulosclerosis, Focal Segmental http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19535569&form=6&db=m ADAM17 upregulation in human renal disease: a role in modulating TGF-alpha availability? therapeutic application,unassigned 1,0 3.4.24.86 Gram-Negative Bacterial Infections http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20154226&form=6&db=m In vivo role of leukocyte ADAM17 in the inflammatory and host responses during E. coli-mediated peritonitis. causal interaction,ongoing research,therapeutic application,unassigned 4,2,1,0 3.4.24.86 Graves Disease http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22506015&form=6&db=m Nuclear targeting of IGF-1 receptor in orbital fibroblasts from Graves' disease: apparent role of ADAM17. causal interaction,ongoing research,unassigned 3,1,0 3.4.24.86 Head and Neck Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18483276&form=6&db=m The soluble alpha chain of interleukin-15 receptor: a proinflammatory molecule associated with tumor progression in head and neck cancer. causal interaction,diagnostic usage,ongoing research,unassigned 1,2,2,0 3.4.24.86 Head Injuries, Closed http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26939762&form=6&db=m Distinct roles for metalloproteinases during traumatic brain injury. causal interaction,diagnostic usage,unassigned 4,2,0 3.4.24.86 Heart Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20184396&form=6&db=m ADAM-17: the enzyme that does it all. causal interaction,therapeutic application,unassigned 4,1,0 3.4.24.86 Heart Failure http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15556048&form=6&db=m Increased expression of tumor necrosis factor-alpha converting enzyme and tumor necrosis factor-alpha in peripheral blood mononuclear cells in patients with advanced congestive heart failure. causal interaction,diagnostic usage,ongoing research,unassigned 3,3,3,0 3.4.24.86 Heart Failure http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33660945&form=6&db=m Pulmonary, cardiac and renal distribution of ACE2, furin, TMPRSS2 and ADAM17 in rats with heart failure: Potential implication for COVID-19 disease. causal interaction,diagnostic usage,ongoing research,unassigned 3,3,4,0 3.4.24.86 Hepatitis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20628198&form=6&db=m Ectodomain shedding of EGFR ligands and TNFR1 dictates hepatocyte apoptosis during fulminant hepatitis in mice. causal interaction,ongoing research,unassigned 1,2,0 3.4.24.86 Hepatitis, Alcoholic http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29980709&form=6&db=m Iron-Overload triggers ADAM-17 mediated inflammation in Severe Alcoholic Hepatitis. causal interaction,unassigned 2,0 3.4.24.86 HIV Infections http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27773542&form=6&db=m HIV Nef- and Notch1-dependent Endocytosis of ADAM17 Induces Vesicular TNF Secretion in Chronic HIV Infection. causal interaction,diagnostic usage,ongoing research,unassigned 2,1,1,0 3.4.24.86 Hyperglycemia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23646149&form=6&db=m Rosiglitazone treatment of type 2 diabetic db/db mice attenuates urinary albumin and angiotensin converting enzyme 2 excretion. ongoing research,therapeutic application,unassigned 4,1,0 3.4.24.86 Hyperglycemia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23678045&form=6&db=m ADAM17 mediates Nox4 expression and NADPH oxidase activity in the kidney cortex of OVE26 mice. causal interaction,unassigned 4,0 3.4.24.86 Hyperparathyroidism, Primary http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29056164&form=6&db=m ADAM17, a New Player in the Pathogenesis of Chronic Kidney Disease-Mineral and Bone Disorder. causal interaction,diagnostic usage,ongoing research,unassigned 4,2,2,0 3.4.24.86 Hyperparathyroidism, Secondary http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33715866&form=6&db=m Contribution of phosphorus and PTH to the development of cardiac hypertrophy and fibrosis in an experimental model of chronic renal failure. causal interaction,unassigned 3,0 3.4.24.86 Hypersensitivity http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30586315&form=6&db=m Impaired mechanical, heat, and cold nociception in a murine model of genetic TACE/ADAM17 knockdown. causal interaction,therapeutic application,unassigned 4,2,0 3.4.24.86 Hypertension http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24014829&form=6&db=m Brain ACE2 Shedding Contributes to the Development of Neurogenic Hypertension. causal interaction,therapeutic application,unassigned 3,1,0 3.4.24.86 Hypertension http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24871629&form=6&db=m Vascular Induction of a Disintegrin and Metalloprotease 17 by Angiotensin II Through Hypoxia Inducible Factor 1? causal interaction,therapeutic application,unassigned 3,1,0 3.4.24.86 Hypertension http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25801471&form=6&db=m The compensatory renin-angiotensin system in the central regulation of arterial pressure: new avenues and new challenges. causal interaction,therapeutic application,unassigned 4,4,0 3.4.24.86 Hypertension http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25916723&form=6&db=m Role of epidermal growth factor receptor and endoplasmic reticulum stress in vascular remodeling induced by angiotensin II. causal interaction,therapeutic application,unassigned 4,4,0 3.4.24.86 Hypertension http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26254330&form=6&db=m ?-Lipoic acid reduces neurogenic hypertension by blunting oxidative stress-mediated increase in ADAM17. causal interaction,ongoing research,therapeutic application,unassigned 4,2,1,0 3.4.24.86 Hypertension http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26514426&form=6&db=m Cilostazol inhibits interleukin-1-induced ADAM17 expression through cAMP independent signaling in vascular smooth muscle cells. causal interaction,unassigned 3,0 3.4.24.86 Hypertension http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26598506&form=6&db=m TRPC3 channel confers cerebrovascular remodelling during hypertension via transactivation of EGF receptor signalling. causal interaction,unassigned 1,0 3.4.24.86 Hypertension http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27480833&form=6&db=m Vascular ADAM17 as a Novel Therapeutic Target in Mediating Cardiovascular Hypertrophy and Perivascular Fibrosis Induced by Angiotensin II. causal interaction,therapeutic application,unassigned 1,3,0 3.4.24.86 Hypertension http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27993561&form=6&db=m Loss of smooth muscle cell disintegrin and metalloproteinase 17 transiently suppresses angiotensin II-induced hypertension and end-organ damage. causal interaction,ongoing research,therapeutic application,unassigned 1,4,1,0 3.4.24.86 Hypertension http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28512108&form=6&db=m Clinical Relevance and Role of Neuronal AT1 Receptors in ADAM17-Mediated ACE2 Shedding in Neurogenic Hypertension. causal interaction,diagnostic usage,ongoing research,unassigned 3,4,3,0 3.4.24.86 Hypertension http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31006330&form=6&db=m Activation of ADAM17 (A Disintegrin and Metalloprotease 17) on Glutamatergic Neurons Selectively Promotes Sympathoexcitation. causal interaction,diagnostic usage,ongoing research,therapeutic application 2,2,4,1 3.4.24.86 Hypertension http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31141400&form=6&db=m Role of ADAM17 in kidney disease. causal interaction,ongoing research,therapeutic application,unassigned 4,3,4,0 3.4.24.86 Hypertension http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31564162&form=6&db=m ACE2 and ADAM17 Interaction Regulates the Activity of Presympathetic Neurons. ongoing research,unassigned 4,0 3.4.24.86 Hypertension http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32762876&form=6&db=m Lung ACE2 and ADAM17 in pulmonary arterial hypertension: Implications for COVID-19? causal interaction,therapeutic application,unassigned 2,2,0 3.4.24.86 Hypertension http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32848763&form=6&db=m ADAM17-Mediated Shedding of Inflammatory Cytokines in Hypertension. causal interaction,ongoing research,therapeutic application,unassigned 3,2,1,0 3.4.24.86 Hypertension http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33330676&form=6&db=m The Role of iRhom2 in Metabolic and Cardiovascular-Related Disorders. causal interaction,therapeutic application,unassigned 4,1,0 3.4.24.86 Hypertension http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34419773&form=6&db=m Which ones, when and why should renin-angiotensin system inhibitors work against COVID-19? causal interaction,unassigned 3,0 3.4.24.86 Hypopharyngeal Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32889897&form=6&db=m MiR-338-3p inhibits cell migration and invasion in human hypopharyngeal cancer via downregulation of ADAM17. causal interaction,ongoing research,therapeutic application,unassigned 4,3,4,0 3.4.24.86 Hypothalamic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16399672&form=6&db=m Hypothalamic tumor necrosis factor-alpha converting enzyme mediates excitatory amino acid-dependent neuron-to-glia signaling in the neuroendocrine brain. unassigned - 3.4.24.86 Idiopathic Pulmonary Fibrosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31469350&form=6&db=m Association of ADAM17 Expression Levels in Patients with Interstitial Lung Disease. causal interaction,diagnostic usage,ongoing research,unassigned 4,4,4,0 3.4.24.86 Infarction, Middle Cerebral Artery http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=14960606&form=6&db=m In vitro ischemic tolerance involves upregulation of glutamate transport partly mediated by the TACE/ADAM17-tumor necrosis factor-alpha pathway. unassigned - 3.4.24.86 Infections http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19816567&form=6&db=m MUC1 limits Helicobacter pylori infection both by steric hindrance and by acting as a releasable decoy. unassigned - 3.4.24.86 Infections http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20303353&form=6&db=m Helicobacter pylori CagL Activates ADAM17 to Induce Repression of the Gastric H, K-ATPase alpha Subunit. unassigned - 3.4.24.86 Infections http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22623356&form=6&db=m ADAM17 activation in circulating neutrophils following bacterial challenge impairs their recruitment. causal interaction,ongoing research,therapeutic application,unassigned 3,2,2,0 3.4.24.86 Infections http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23349873&form=6&db=m ATP-mediated transactivation of the epidermal growth factor receptor in airway epithelial cells involves DUOX1-dependent oxidation of Src and ADAM17. causal interaction,unassigned 4,0 3.4.24.86 Infections http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23688779&form=6&db=m ADAM17 silencing by adenovirus encoding miRNA-embedded siRNA revealed essential signal transduction by angiotensin II in vascular smooth muscle cells. ongoing research,therapeutic application,unassigned 1,1,0 3.4.24.86 Infections http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24330735&form=6&db=m Analysis of cell hyperplasia and parietal cell dysfunction induced by Ostertagia ostertagi infection. unassigned - 3.4.24.86 Infections http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24965453&form=6&db=m Modulation of CD163 expression by metalloprotease ADAM17 regulates porcine reproductive and respiratory syndrome virus entry. causal interaction,ongoing research,unassigned 4,1,0 3.4.24.86 Infections http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25412102&form=6&db=m Shed GP of Ebola virus triggers immune activation and increased vascular permeability. causal interaction,ongoing research,unassigned 1,1,0 3.4.24.86 Infections http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26019295&form=6&db=m Shedding of TNF receptor 2 by effector CD8? T cells by ADAM17 is important for regulating TNF-? availability during influenza infection. therapeutic application,unassigned 1,0 3.4.24.86 Infections http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26561568&form=6&db=m ADAM17 controls IL-6 signaling by cleavage of the murine IL-6R? from the cell surface of leukocytes during inflammatory responses. unassigned - 3.4.24.86 Infections http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27256961&form=6&db=m Regulation of A disintegrin and metalloproteinase (ADAM) family sheddases ADAM10 and ADAM17: The emerging role of tetraspanins and rhomboids. causal interaction,unassigned 1,0 3.4.24.86 Infections http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27381289&form=6&db=m Ehrlichia chaffeensis TRP120 Activates Canonical Notch Signaling To Downregulate TLR2/4 Expression and Promote Intracellular Survival. causal interaction,unassigned 2,0 3.4.24.86 Infections http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27784899&form=6&db=m Plasma Ang2 and ADAM17 levels are elevated during clinical malaria; Ang2 level correlates with severity and expression of EPCR-binding PfEMP1. causal interaction,diagnostic usage,ongoing research,unassigned 4,2,3,0 3.4.24.86 Infections http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28487846&form=6&db=m Ectodomain Shedding by ADAM17: Its Role in Neutrophil Recruitment and the Impairment of This Process during Sepsis. causal interaction,ongoing research,therapeutic application,unassigned 3,2,1,0 3.4.24.86 Infections http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29475600&form=6&db=m Metalloprotease ADAM17 regulates porcine epidemic diarrhea virus infection by modifying aminopeptidase N. causal interaction,ongoing research,therapeutic application,unassigned 3,2,2,0 3.4.24.86 Infections http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30371773&form=6&db=m Expression levels of A disintegrin and metalloproteases (ADAMs), and Th17-related cytokines and their association with Helicobacter pylori infection in patients with gastroduodenal diseases. causal interaction,diagnostic usage,ongoing research,unassigned 2,4,2,0 3.4.24.86 Infections http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30616034&form=6&db=m Decoding the enigma of antiviral crisis: Does one target molecule regulate all? causal interaction,ongoing research,therapeutic application,unassigned 3,2,4,0 3.4.24.86 Infections http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32385608&form=6&db=m Tetraspanin CD9 affects HPV16 infection by modulating ADAM17 activity and the ERK signalling pathway. therapeutic application,unassigned 1,0 3.4.24.86 Infections http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32401783&form=6&db=m TREM2 suppresses the proinflammatory response to facilitate PRRSV infection via PI3K/NF-?B signaling. unassigned - 3.4.24.86 Infections http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32769398&form=6&db=m Shedding Light on COVID-19: ADAM17 the Missing Link? causal interaction,diagnostic usage,ongoing research,therapeutic application 3,1,1,4 3.4.24.86 Infections http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33199671&form=6&db=m Expression Analyses of MicroRNAs in Hamster Lung Tissues Infected by SARS-CoV-2. causal interaction,unassigned 4,0 3.4.24.86 Infections http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34410424&form=6&db=m Instigators of COVID-19 in Immune Cells are Increased in Tobacco Cigarette Smokers and Electronic Cigarette Vapers Compared to Non-smokers. causal interaction,ongoing research,unassigned 1,2,0 3.4.24.86 Inflammatory Bowel Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22236242&form=6&db=m Inflammatory bowel disease and ADAM17 deletion. diagnostic usage,unassigned 3,0 3.4.24.86 Influenza, Human http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26019295&form=6&db=m Shedding of TNF receptor 2 by effector CD8? T cells by ADAM17 is important for regulating TNF-? availability during influenza infection. therapeutic application,unassigned 1,0 3.4.24.86 Insulin Resistance http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17646208&form=6&db=m Mice heterozygous for tumor necrosis factor-alpha converting enzyme are protected from obesity-induced insulin resistance and diabetes. ongoing research,therapeutic application,unassigned 3,2,0 3.4.24.86 Insulin Resistance http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19154693&form=6&db=m [The two sides of ADAM17 in inflammation: implications in atherosclerosis and obesity] causal interaction,therapeutic application,unassigned 4,1,0 3.4.24.86 Insulin Resistance http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19819120&form=6&db=m ADAM17_i33708A>G polymorphism interacts with dietary n-6 polyunsaturated fatty acids to modulate obesity risk in the Genetics of Lipid Lowering Drugs and Diet Network study. causal interaction,diagnostic usage,ongoing research,unassigned 4,2,2,0 3.4.24.86 Insulin Resistance http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19877183&form=6&db=m Increased tumor necrosis factor alpha-converting enzyme activity induces insulin resistance and hepatosteatosis in mice. causal interaction,therapeutic application,unassigned 4,1,0 3.4.24.86 Insulin Resistance http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23384719&form=6&db=m The role of ADAM17 in metabolic inflammation. causal interaction,unassigned 4,0 3.4.24.86 Insulin Resistance http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29159092&form=6&db=m Discriminatory metabolic and inflammatory parameters in serum and omental adipose tissue of obese patients with different insulin sensitivity. causal interaction,diagnostic usage,unassigned 1,4,0 3.4.24.86 Insulin Resistance http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34318951&form=6&db=m WITHDRAWN: Adipocyte Deletion of ADAM17 Leads to Insulin Resistance in Association with Age and HFD in Mice. ongoing research,unassigned 3,0 3.4.24.86 Intestinal Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29472497&form=6&db=m ADAM17 is required for EGF-R-induced intestinal tumors via IL-6 trans-signaling. causal interaction,ongoing research,therapeutic application,unassigned 4,3,4,0 3.4.24.86 Intestinal Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31060243&form=6&db=m Functional Characterization of Colon Cancer-Associated Mutations in ADAM17: Modifications in the Pro-Domain Interfere with Trafficking and Maturation. causal interaction,ongoing research,unassigned 2,3,0 3.4.24.86 Intestinal Volvulus http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16273118&form=6&db=m Human colonic myocytes are involved in postischemic inflammation through ADAM17-dependent TNFalpha production. ongoing research,therapeutic application,unassigned 1,1,0 3.4.24.86 Iron Overload http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33683629&form=6&db=m The Effect of TCM-Induced HAMP on Key Enzymes in the Hydrolysis of AD Model Cells. ongoing research,unassigned 1,0 3.4.24.86 Ischemic Stroke http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23771674&form=6&db=m Changes in platelet GPIb? and ADAM17 during the acute stage of atherosclerotic ischemic stroke among Chinese. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,2,3,4 3.4.24.86 Ischemic Stroke http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24727681&form=6&db=m Association between ADAM17 Promoter Polymorphisms and Ischemic Stroke in a Chinese Population. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,2,3,1 3.4.24.86 Joint Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15920158&form=6&db=m Lack of tissue inhibitor of metalloproteinases-3 results in an enhanced inflammatory response in antigen-induced arthritis. causal interaction,therapeutic application,unassigned 1,1,0 3.4.24.86 Joint Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31369701&form=6&db=m Novel functions of inactive rhomboid proteins in immunity and disease. causal interaction,unassigned 3,0 3.4.24.86 Keloid http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34502327&form=6&db=m Multi-Antigen Imaging Reveals Inflammatory DC, ADAM17 and Neprilysin as Effectors in Keloid Formation. causal interaction,unassigned 2,0 3.4.24.86 Keratoderma, Palmoplantar, Diffuse http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24738885&form=6&db=m Insights into desmosome biology from inherited human skin disease and cardiocutaneous syndromes. unassigned - 3.4.24.86 Kidney Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19435795&form=6&db=m CXCL16 Is Expressed in Podocytes and Acts as a Scavenger Receptor for Oxidized Low-Density Lipoprotein. causal interaction,therapeutic application,unassigned 3,4,0 3.4.24.86 Kidney Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25294851&form=6&db=m The induction of C/EBP? contributes to vitamin D inhibition of ADAM17 expression and parathyroid hyperplasia in kidney disease. causal interaction,ongoing research,unassigned 3,1,0 3.4.24.86 Kidney Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31141400&form=6&db=m Role of ADAM17 in kidney disease. causal interaction,ongoing research,therapeutic application,unassigned 4,3,4,0 3.4.24.86 Kidney Diseases, Cystic http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24899059&form=6&db=m ADAM17 promotes proliferation of collecting duct kidney epithelial cells through ERK activation and increased glycolysis in polycystic kidney disease. causal interaction,diagnostic usage,ongoing research,unassigned 1,3,4,0 3.4.24.86 Kidney Failure, Chronic http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26970513&form=6&db=m Association of CD30 transcripts with Th1 responses and proinflammatory cytokines in patients with end-stage renal disease. diagnostic usage,ongoing research,unassigned 3,1,0 3.4.24.86 Kidney Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19190330&form=6&db=m Human renal cancer cells express a novel membrane-bound interleukin-15 that induces, in response to the soluble interleukin-15 receptor alpha chain, epithelial-to-mesenchymal transition. unassigned - 3.4.24.86 Kidney Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23441135&form=6&db=m MicroRNA-145 Targets the Metalloprotease ADAM17 and Is Suppressed in Renal Cell Carcinoma Patients. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,1,2,1 3.4.24.86 Klatskin Tumor http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29776401&form=6&db=m ADAM-17 is a poor prognostic indicator for patients with hilar cholangiocarcinoma and is regulated by FoxM1. causal interaction,diagnostic usage,ongoing research,unassigned 3,4,4,0 3.4.24.86 Leukemia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16497166&form=6&db=m Modulation of autocrine TNF-alpha-stimulated matrix metalloproteinase 9 (MMP-9) expression by mitogen-activated protein kinases in THP-1 monocytic cells. causal interaction,ongoing research,therapeutic application,unassigned 4,1,3,0 3.4.24.86 Leukemia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16806998&form=6&db=m High molecular weight hyaluronic acid down-regulates the gene expression of osteoarthritis-associated cytokines and enzymes in fibroblast-like synoviocytes from patients with early osteoarthritis. ongoing research,unassigned 3,0 3.4.24.86 Leukemia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19704010&form=6&db=m Selective use of ADAM10 and ADAM17 in activation of Notch1 signaling. causal interaction,unassigned 1,0 3.4.24.86 Leukemia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22705645&form=6&db=m Suppression of Akt/Foxp3-mediated miR-183 expression blocks Sp1-mediated ADAM17 expression and TNF?-mediated NF?B activation in piceatannol-treated human leukemia U937 cells. ongoing research,unassigned 3,0 3.4.24.86 Leukemia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23791922&form=6&db=m Hydroquinone-induced miR-122 down-regulation elicits ADAM17 up-regulation, leading to increased soluble TNF-? production in human leukemia cells with expressed Bcr/Abl. ongoing research,unassigned 2,0 3.4.24.86 Leukemia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24874889&form=6&db=m Taiwan cobra phospholipase A2 suppresses ERK-mediated ADAM17 maturation, thus reducing secreted TNF-? production in human leukemia U937 cells. ongoing research,unassigned 4,0 3.4.24.86 Leukemia, Myeloid, Acute http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23690482&form=6&db=m Targeting natural killer cells to acute myeloid leukemia in vitro with a CD16 x 33 bispecific killer cell engager and ADAM17 inhibition. unassigned - 3.4.24.86 Listeriosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28877252&form=6&db=m The role of ADAM17 in the T-cell response against bacterial pathogens. therapeutic application,unassigned 2,0 3.4.24.86 Liver Cirrhosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15309730&form=6&db=m ADAM17 mRNA expression and pathological features of hepatocellular carcinoma. causal interaction,diagnostic usage,ongoing research,unassigned 1,4,4,0 3.4.24.86 Liver Cirrhosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19432809&form=6&db=m CX3CL1/FRACTALKINE SHEDDING BY HUMAN HEPATIC STELLATE CELLS: CONTRIBUTION TO CHRONIC INFLAMMATION IN THE LIVER. causal interaction,ongoing research,unassigned 3,1,0 3.4.24.86 Liver Cirrhosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31662486&form=6&db=m iRhom2 inhibits bile duct obstruction-induced liver fibrosis. ongoing research,unassigned 4,0 3.4.24.86 Liver Cirrhosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34075077&form=6&db=m ADAM10 and ADAM17 regulate EGFR, c-Met and TNF RI signalling in liver regeneration and fibrosis. causal interaction,unassigned 4,0 3.4.24.86 Liver Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19432809&form=6&db=m CX3CL1/FRACTALKINE SHEDDING BY HUMAN HEPATIC STELLATE CELLS: CONTRIBUTION TO CHRONIC INFLAMMATION IN THE LIVER. causal interaction,ongoing research,unassigned 3,1,0 3.4.24.86 Liver Failure http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20628198&form=6&db=m Ectodomain shedding of EGFR ligands and TNFR1 dictates hepatocyte apoptosis during fulminant hepatitis in mice. causal interaction,ongoing research,unassigned 1,2,0 3.4.24.86 Liver Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25174729&form=6&db=m MicroRNA-145 inhibits cell proliferation by directly targeting ADAM17 in hepatocellular carcinoma. therapeutic application,unassigned 1,0 3.4.24.86 Liver Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26993601&form=6&db=m Role of ADAM17 in invasion and migration of CD133-expressing liver cancer stem cells after irradiation. causal interaction,diagnostic usage,ongoing research,unassigned 1,3,3,0 3.4.24.86 Liver Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30297396&form=6&db=m iNOS promotes CD24+CD133+ liver cancer stem cell phenotype through a TACE/ADAM17-dependent Notch signaling pathway. causal interaction,diagnostic usage,therapeutic application,unassigned 4,3,1,0 3.4.24.86 Lung Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34208027&form=6&db=m The Role of CX3CL1 and ADAM17 in Pathogenesis of Diffuse Parenchymal Lung Diseases. causal interaction,diagnostic usage,ongoing research,unassigned 3,1,2,0 3.4.24.86 Lung Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34410424&form=6&db=m Instigators of COVID-19 in Immune Cells are Increased in Tobacco Cigarette Smokers and Electronic Cigarette Vapers Compared to Non-smokers. causal interaction,ongoing research,unassigned 1,2,0 3.4.24.86 Lung Diseases, Interstitial http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29411180&form=6&db=m ADAM-17 is expressed in the inflammatory myopathy and is involved with interstitial lung disease. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,4,4 3.4.24.86 Lung Diseases, Interstitial http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29525842&form=6&db=m Correction to: ADAM-17 is expressed in the inflammatory myopathy and is involved with interstitial lung disease. causal interaction,unassigned 4,0 3.4.24.86 Lung Diseases, Interstitial http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31469350&form=6&db=m Association of ADAM17 Expression Levels in Patients with Interstitial Lung Disease. causal interaction,diagnostic usage,ongoing research,unassigned 4,4,4,0 3.4.24.86 Lung Diseases, Interstitial http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34208027&form=6&db=m The Role of CX3CL1 and ADAM17 in Pathogenesis of Diffuse Parenchymal Lung Diseases. causal interaction,diagnostic usage,ongoing research,unassigned 3,1,2,0 3.4.24.86 Lung Injury http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17172985&form=6&db=m Nonischemic lung injury by mediators from unilateral ischemic reperfused lung: ameliorating effect of tumor necrosis factor-alpha-converting enzyme inhibitor. causal interaction,ongoing research,unassigned 2,2,0 3.4.24.86 Lung Injury http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21247898&form=6&db=m Neuregulin-1-human epidermal receptor-2 signaling is a central regulator of pulmonary epithelial permeability and acute lung injury. unassigned - 3.4.24.86 Lung Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19776420&form=6&db=m Identification of five candidate lung cancer biomarkers by proteomic analysis of conditioned media of four lung cancer cell lines. diagnostic usage,ongoing research,unassigned 2,3,0 3.4.24.86 Lung Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20551051&form=6&db=m ADAM17 regulates epidermal growth factor receptor expression through the activation of Notch1 in non-small cell lung cancer. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,3,3 3.4.24.86 Lung Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22291012&form=6&db=m Lung cancer-derived galectin-1 enhances tumorigenic potentiation of tumor associated dendritic cells by expressing HB-EGF. ongoing research,therapeutic application,unassigned 1,1,0 3.4.24.86 Lung Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22509934&form=6&db=m A novel bispecific single-chain antibody for ADAM17 and CD3 induces T-cell-mediated lysis of prostate cancer cells. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,3,4,1 3.4.24.86 Lung Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23475633&form=6&db=m ADAM17 is overexpressed in non-small cell lung cancer and its expression correlates with poor patient survival. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,4,3 3.4.24.86 Lung Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24626788&form=6&db=m ADAM17 silencing suppresses the migration and invasion of non-small cell lung cancer. causal interaction,ongoing research,therapeutic application,unassigned 3,3,1,0 3.4.24.86 Lung Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25363527&form=6&db=m Estrogen upregulates MICA/B expression in human non-small cell lung cancer through the regulation of ADAM17. ongoing research,therapeutic application,unassigned 2,1,0 3.4.24.86 Lung Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27076628&form=6&db=m Secretome Signature Identifies ADAM17 as Novel Target for Radiosensitization of Non-Small Cell Lung Cancer. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,3,4,4 3.4.24.86 Lung Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27618869&form=6&db=m Savior or not: ADAM17 inhibitors overcome radiotherapy-resistance in non-small cell lung cancer. therapeutic application,unassigned 3,0 3.4.24.86 Lung Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29308299&form=6&db=m Platelet-mediated shedding of NKG2D ligands impairs NK cell immune-surveillance of tumor cells. causal interaction,diagnostic usage,unassigned 1,1,0 3.4.24.86 Lung Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30617444&form=6&db=m Sema4D expression and secretion are increased by HIF-1? and inhibit osteogenesis in bone metastases of lung cancer. causal interaction,diagnostic usage,unassigned 3,3,0 3.4.24.86 Lung Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30833304&form=6&db=m ADAM17 selectively activates the IL-6 trans-signaling/ERK MAPK axis in KRAS-addicted lung cancer. ongoing research,therapeutic application,unassigned 1,4,0 3.4.24.86 Lung Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31438559&form=6&db=m ADAM17: An Emerging Therapeutic Target for Lung Cancer. causal interaction,therapeutic application,unassigned 3,4,0 3.4.24.86 Lung Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31442576&form=6&db=m Novel ADAM-17 inhibitor ZLDI-8 inhibits the proliferation and metastasis of chemo-resistant non-small-cell lung cancer by reversing Notch and epithelial mesenchymal transition in vitro and in vivo. ongoing research,unassigned 2,0 3.4.24.86 Lupus Nephritis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31369701&form=6&db=m Novel functions of inactive rhomboid proteins in immunity and disease. causal interaction,unassigned 3,0 3.4.24.86 Lymphatic Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17438092&form=6&db=m ADAM-17 expression in breast cancer correlates with variables of tumor progression. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,4,2 3.4.24.86 Lymphatic Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18238782&form=6&db=m ADAM-17 predicts adverse outcome in patients with breast cancer. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,4,3 3.4.24.86 Lymphatic Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22139867&form=6&db=m Prognostic value of ADAM17 in human gastric cancer. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,4,3 3.4.24.86 Lymphatic Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23475633&form=6&db=m ADAM17 is overexpressed in non-small cell lung cancer and its expression correlates with poor patient survival. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,4,3 3.4.24.86 Lymphatic Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24793016&form=6&db=m ADAM17 is associated with EMMPRIN and predicts poor prognosis in patients with uterine cervical carcinoma. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,4,3 3.4.24.86 Lymphatic Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25351873&form=6&db=m A disintegrin and metalloproteinase 17 mRNA and protein expression in esophageal squamous cell carcinoma, as well as its clinicopathological factors and prognosis. causal interaction,diagnostic usage,ongoing research,unassigned 3,4,4,0 3.4.24.86 Lymphatic Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25786367&form=6&db=m Prognostic significance of ADAM17 expression in patients with gastric cancer who underwent curative gastrectomy. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,4,2 3.4.24.86 Lymphatic Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25966212&form=6&db=m Expression and clinical significance of ADAM17 protein in esophageal squamous cell carcinoma. causal interaction,diagnostic usage,ongoing research,unassigned 1,4,4,0 3.4.24.86 Lymphatic Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30569104&form=6&db=m ADAM17 promotes lymph node metastasis in gastric cancer via activation of the Notch and Wnt signaling pathways. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,3,1 3.4.24.86 Lymphatic Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32610677&form=6&db=m Prognostic Significance of ADAM17 for Gastric Cancer Survival: A Meta-Analysis. causal interaction,diagnostic usage,therapeutic application,unassigned 4,4,3,0 3.4.24.86 Macular Degeneration http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34509473&form=6&db=m ADAM17 mediates ectodomain shedding of the soluble VLDL receptor fragment in the retinal epithelium. causal interaction,unassigned 2,0 3.4.24.86 Malaria http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27784899&form=6&db=m Plasma Ang2 and ADAM17 levels are elevated during clinical malaria; Ang2 level correlates with severity and expression of EPCR-binding PfEMP1. causal interaction,diagnostic usage,ongoing research,unassigned 4,2,3,0 3.4.24.86 Massive Hepatic Necrosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20628198&form=6&db=m Ectodomain shedding of EGFR ligands and TNFR1 dictates hepatocyte apoptosis during fulminant hepatitis in mice. causal interaction,ongoing research,unassigned 1,2,0 3.4.24.86 Melanoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18971959&form=6&db=m ADAM10 is the constitutive functional sheddase of CD44 in human melanoma cells. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,3,4,1 3.4.24.86 Melanoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19003995&form=6&db=m UV-induced EGFR signal transactivation is dependent on proligand shedding by activated metalloproteases in skin cancer cell lines. causal interaction,ongoing research,unassigned 1,2,0 3.4.24.86 Melanoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19434087&form=6&db=m Shedding light on proteolytic cleavage of CD44: the responsible sheddase and functional significance of shedding. ongoing research,therapeutic application,unassigned 2,1,0 3.4.24.86 Melanoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23645517&form=6&db=m Molecular Profiling of ADAM12 and ADAM17 Genes in Human Malignant Melanoma. causal interaction,diagnostic usage,ongoing research,unassigned 4,4,4,0 3.4.24.86 Melanoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34224305&form=6&db=m Rosmarinic acid inhibits proliferation and migration, promotes apoptosis and enhances cisplatin sensitivity of melanoma cells through inhibiting ADAM17/EGFR/AKT/GSK3? axis. ongoing research,therapeutic application,unassigned 4,1,0 3.4.24.86 Meningitis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12015459&form=6&db=m Current concepts in the pathogenesis of meningitis caused by Streptococcus pneumoniae. causal interaction,therapeutic application,unassigned 3,4,0 3.4.24.86 Meningitis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17428319&form=6&db=m Adjuvant TACE inhibitor treatment improves the outcome of TLR2-/- mice with experimental pneumococcal meningitis. therapeutic application,unassigned 4,0 3.4.24.86 Meningitis, Bacterial http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15145598&form=6&db=m In pneumococcal meningitis a novel water-soluble inhibitor of matrix metalloproteinases and TNF-alpha converting enzyme attenuates seizures and injury of the cerebral cortex. therapeutic application,unassigned 3,0 3.4.24.86 Meningitis, Bacterial http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16790761&form=6&db=m Doxycycline reduces mortality and injury to the brain and cochlea in experimental pneumococcal meningitis. causal interaction,unassigned 4,0 3.4.24.86 Meningitis, Pneumococcal http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15145598&form=6&db=m In pneumococcal meningitis a novel water-soluble inhibitor of matrix metalloproteinases and TNF-alpha converting enzyme attenuates seizures and injury of the cerebral cortex. therapeutic application,unassigned 3,0 3.4.24.86 Metabolic Syndrome http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21406565&form=6&db=m Plasminogen activator inhibitor 1 is an intracellular inhibitor of furin proprotein convertase. causal interaction,diagnostic usage,unassigned 3,3,0 3.4.24.86 Metabolic Syndrome http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33904577&form=6&db=m Implications of ADAM17 activation for hyperglycaemia, obesity and type 2 diabetes. causal interaction,ongoing research,therapeutic application,unassigned 3,2,4,0 3.4.24.86 Mouth Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24403253&form=6&db=m ADAM17-mediated CD44 cleavage promotes orasphere formation or stemness and tumorigenesis in HNSCC. causal interaction,diagnostic usage,ongoing research,therapeutic application 1,4,4,1 3.4.24.86 Mucocutaneous Lymph Node Syndrome http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26833052&form=6&db=m Genetic variants of ADAM17 are implicated in the pathological process of Kawasaki disease and secondary coronary artery lesions via the TGF-?/SMAD3 signaling pathway. causal interaction,unassigned 2,0 3.4.24.86 Multiple Sclerosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16511637&form=6&db=m TNF-alpha converting enzyme (TACE) protein expression in different clinical subtypes of multiple sclerosis. diagnostic usage,ongoing research,unassigned 1,1,0 3.4.24.86 Multiple Sclerosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16900751&form=6&db=m Upregulation of ADAM-17 expression in active lesions in multiple sclerosis. causal interaction,ongoing research,unassigned 4,3,0 3.4.24.86 Multiple Sclerosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19324423&form=6&db=m Expression of ADAM-17, TIMP-3 and fractalkine in the human adult brain endothelial cell line, hCMEC/D3, following pro-inflammatory cytokine treatment. causal interaction,unassigned 3,0 3.4.24.86 Myocardial Infarction http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18226043&form=6&db=m The expression of TNF-alpha converting enzyme at the site of ruptured plaques in patients with acute myocardial infarction. causal interaction,diagnostic usage,therapeutic application,unassigned 4,1,1,0 3.4.24.86 Myocardial Infarction http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26136458&form=6&db=m Cardiomyocyte A Disintegrin And Metalloproteinase 17 (ADAM17) Is Essential in Post-Myocardial Infarction Repair by Regulating Angiogenesis. causal interaction,ongoing research,unassigned 2,4,0 3.4.24.86 Myocardial Infarction http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26944439&form=6&db=m Enhanced ADAM17 expression is associated with cardiac remodeling in rats with acute myocardial infarction. causal interaction,unassigned 4,0 3.4.24.86 Myocardial Infarction http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32170604&form=6&db=m Effect of miR-26a-5p targeting ADAM17 gene on apoptosis, inflammatory factors and oxidative stress response of myocardial cells in hypoxic model. causal interaction,therapeutic application,unassigned 4,2,0 3.4.24.86 Myocardial Infarction http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33492555&form=6&db=m MiR-708-3p Alleviates Inflammation and Myocardial Injury After Myocardial Infarction by Suppressing ADAM17 Expression. causal interaction,unassigned 3,0 3.4.24.86 Myocardial Infarction http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33603264&form=6&db=m Syzygium Polyanthum Reduced TNF-? and ADAM17 Protein Expression in Myocardial Infarction Rat Model. causal interaction,ongoing research,unassigned 1,2,0 3.4.24.86 Myocarditis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11028485&form=6&db=m Expression of tumor necrosis factor-alpha--converting enzyme and tumor necrosis factor-alpha in human myocarditis. causal interaction,diagnostic usage,ongoing research,unassigned 3,4,4,0 3.4.24.86 Myositis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17207628&form=6&db=m The cell-specific expression of metalloproteinase-disintegrins (ADAMs) in inflammatory myopathies. diagnostic usage,ongoing research,therapeutic application,unassigned 3,4,2,0 3.4.24.86 Myositis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29411180&form=6&db=m ADAM-17 is expressed in the inflammatory myopathy and is involved with interstitial lung disease. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,4,4 3.4.24.86 Myositis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29525842&form=6&db=m Correction to: ADAM-17 is expressed in the inflammatory myopathy and is involved with interstitial lung disease. causal interaction,unassigned 4,0 3.4.24.86 Myositis, Inclusion Body http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17207628&form=6&db=m The cell-specific expression of metalloproteinase-disintegrins (ADAMs) in inflammatory myopathies. diagnostic usage,ongoing research,therapeutic application,unassigned 3,4,2,0 3.4.24.86 Nasal Polyps http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27012683&form=6&db=m Expression of ADAM17 and ADAM10 in nasal polyps. diagnostic usage,ongoing research,unassigned 4,4,0 3.4.24.86 Nasopharyngeal Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26297956&form=6&db=m MiR-145, a microRNA targeting ADAM17, inhibits the invasion and migration of nasopharyngeal carcinoma cells. therapeutic application,unassigned 1,0 3.4.24.86 Neoplasm Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17180679&form=6&db=m ADAM-17 associated with CD44 cleavage and metastasis in oral squamous cell carcinoma. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,2,4,1 3.4.24.86 Neoplasm Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17438092&form=6&db=m ADAM-17 expression in breast cancer correlates with variables of tumor progression. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,4,2 3.4.24.86 Neoplasm Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18238782&form=6&db=m ADAM-17 predicts adverse outcome in patients with breast cancer. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,4,3 3.4.24.86 Neoplasm Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19296470&form=6&db=m MicroRNA-122, a tumor suppressor microRNA that regulates intrahepatic metastasis of hepatocellular carcinoma. causal interaction,diagnostic usage,therapeutic application,unassigned 4,1,3,0 3.4.24.86 Neoplasm Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22139867&form=6&db=m Prognostic value of ADAM17 in human gastric cancer. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,4,3 3.4.24.86 Neoplasm Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22200661&form=6&db=m ADAM17 targets MMP-2 and MMP-9 via EGFR-MEK-ERK pathway activation to promote prostate cancer cell invasion. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,4,3 3.4.24.86 Neoplasm Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22668812&form=6&db=m Upregulated Expression of ADAM17 Is a Prognostic Marker for Patients With Gastric Cancer. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,4,1 3.4.24.86 Neoplasm Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23173124&form=6&db=m The role of microRNA in metastatic colorectal cancer and its significance in cancer prognosis and treatment. causal interaction,diagnostic usage,therapeutic application,unassigned 3,3,4,0 3.4.24.86 Neoplasm Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23475633&form=6&db=m ADAM17 is overexpressed in non-small cell lung cancer and its expression correlates with poor patient survival. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,4,3 3.4.24.86 Neoplasm Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24793016&form=6&db=m ADAM17 is associated with EMMPRIN and predicts poor prognosis in patients with uterine cervical carcinoma. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,4,3 3.4.24.86 Neoplasm Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25351873&form=6&db=m A disintegrin and metalloproteinase 17 mRNA and protein expression in esophageal squamous cell carcinoma, as well as its clinicopathological factors and prognosis. causal interaction,diagnostic usage,ongoing research,unassigned 3,4,4,0 3.4.24.86 Neoplasm Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25786367&form=6&db=m Prognostic significance of ADAM17 expression in patients with gastric cancer who underwent curative gastrectomy. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,4,2 3.4.24.86 Neoplasm Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25912030&form=6&db=m A transmembrane C-terminal fragment of syndecan-1 is generated by the metalloproteinase ADAM17 and promotes lung epithelial tumor cell migration and lung metastasis formation. causal interaction,unassigned 3,0 3.4.24.86 Neoplasm Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25966212&form=6&db=m Expression and clinical significance of ADAM17 protein in esophageal squamous cell carcinoma. causal interaction,diagnostic usage,ongoing research,unassigned 1,4,4,0 3.4.24.86 Neoplasm Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27110571&form=6&db=m Expression of Migration-Related Genes in Human Colorectal Cancer and Activity of a Disintegrin and Metalloproteinase 17. causal interaction,diagnostic usage,ongoing research,unassigned 1,4,4,0 3.4.24.86 Neoplasm Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27573075&form=6&db=m A-Disintegrin and Metalloproteinase (ADAM) 17 Enzymatically Degrades Interferon-gamma. causal interaction,ongoing research,therapeutic application,unassigned 3,3,4,0 3.4.24.86 Neoplasm Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27576135&form=6&db=m Mass spectrometry-based proteomics revealed Glypican-1 as a novel ADAM17 substrate. causal interaction,ongoing research,therapeutic application,unassigned 4,1,2,0 3.4.24.86 Neoplasm Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27874952&form=6&db=m Nox1 promotes colon cancer cell metastasis via activation of the ADAM17 pathway. causal interaction,diagnostic usage,ongoing research,unassigned 3,3,1,0 3.4.24.86 Neoplasm Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27878499&form=6&db=m Therapeutic potential of ADAM17 modulation in gastric cancer through regulation of the EGFR and TNF-? signalling pathways. causal interaction,diagnostic usage,ongoing research,unassigned 4,3,4,0 3.4.24.86 Neoplasm Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29966664&form=6&db=m ADAM17 promotes cell migration and invasion through the integrin ?1 pathway in hepatocellular carcinoma. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,4,4 3.4.24.86 Neoplasm Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30569104&form=6&db=m ADAM17 promotes lymph node metastasis in gastric cancer via activation of the Notch and Wnt signaling pathways. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,3,1 3.4.24.86 Neoplasm Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30617444&form=6&db=m Sema4D expression and secretion are increased by HIF-1? and inhibit osteogenesis in bone metastases of lung cancer. causal interaction,diagnostic usage,unassigned 3,3,0 3.4.24.86 Neoplasm Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31442576&form=6&db=m Novel ADAM-17 inhibitor ZLDI-8 inhibits the proliferation and metastasis of chemo-resistant non-small-cell lung cancer by reversing Notch and epithelial mesenchymal transition in vitro and in vivo. ongoing research,unassigned 2,0 3.4.24.86 Neoplasm Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31978449&form=6&db=m Novel ADAM-17 inhibitor ZLDI-8 inhibits the metastasis of hepatocellular carcinoma by reversing epithelial-mesenchymal transition in vitro and in vivo. ongoing research,therapeutic application,unassigned 4,3,0 3.4.24.86 Neoplasm Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32610677&form=6&db=m Prognostic Significance of ADAM17 for Gastric Cancer Survival: A Meta-Analysis. causal interaction,diagnostic usage,therapeutic application,unassigned 4,4,3,0 3.4.24.86 Neoplasm Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33100908&form=6&db=m ADAM17 promotes the invasion of hepatocellular carcinoma via upregulation MMP21. causal interaction,diagnostic usage,ongoing research,unassigned 4,3,1,0 3.4.24.86 Neoplasm Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34208863&form=6&db=m Regulation of Platelet-Derived ADAM17: A Biomarker Approach for Breast Cancer? causal interaction,therapeutic application,unassigned 4,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8753775&form=6&db=m Relaxed specificity of matrix metalloproteinases (MMPS) and TIMP insensitivity of tumor necrosis factor-alpha (TNF-alpha) production suggest the major TNF-alpha converting enzyme is not an MMP. ongoing research,therapeutic application,unassigned 3,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9428736&form=6&db=m 2 angstrom X-ray structure of adamalysin II complexed with a peptide phosphonate inhibitor adopting a retro-binding mode. ongoing research,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9520379&form=6&db=m Crystal structure of the catalytic domain of human tumor necrosis factor-alpha-converting enzyme. ongoing research,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9521103&form=6&db=m Structures of adamalysin II with peptidic inhibitors. Implications for the design of tumor necrosis factor alpha convertase inhibitors. therapeutic application,unassigned 4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9598327&form=6&db=m Genetic mapping of mouse tumor necrosis factor-alpha converting enzyme (TACE) to chromosome 12. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9733803&form=6&db=m Pro-tumor necrosis factor-alpha processing activity is tightly controlled by a component that does not affect notch processing. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9774383&form=6&db=m Evidence that tumor necrosis factor alpha converting enzyme is involved in regulated alpha-secretase cleavage of the Alzheimer amyloid protein precursor. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9812885&form=6&db=m An essential role for ectodomain shedding in mammalian development. causal interaction,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10093737&form=6&db=m Characterization of the tumour necrosis factor alpha-converting enzyme, TACE/ADAM17. diagnostic usage,ongoing research,unassigned 1,3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10187843&form=6&db=m Unaltered cleavage and secretion of angiotensin-converting enzyme in tumor necrosis factor-alpha-converting enzyme-deficient mice. causal interaction,ongoing research,unassigned 1,3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10375622&form=6&db=m cDNA cloning of mouse tumor necrosis factor-alpha converting enzyme (TACE) and partial analysis of its promoter. diagnostic usage,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10385500&form=6&db=m Tumor necrosis factor-alpha-converting enzyme and tumor necrosis factor-alpha in human dilated cardiomyopathy. ongoing research,unassigned 4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10521439&form=6&db=m Specific sequence elements are required for the expression of functional tumor necrosis factor-alpha-converting enzyme (TACE). causal interaction,diagnostic usage,unassigned 4,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10527948&form=6&db=m Evidence for an interaction of the metalloprotease-disintegrin tumour necrosis factor alpha convertase (TACE) with mitotic arrest deficient 2 (MAD2), and of the metalloprotease-disintegrin MDC9 with a novel MAD2-related protein, MAD2beta. causal interaction,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10579851&form=6&db=m New alpha-substituted succinate-based hydroxamic acids as TNFalpha convertase inhibitors. therapeutic application,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10650948&form=6&db=m Human placental trophoblasts secrete a disintegrin metalloproteinase very similar to the insulin-like growth factor binding protein-3 protease in human pregnancy serum. therapeutic application,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10744726&form=6&db=m Tumor necrosis factor-alpha-converting enzyme is required for cleavage of erbB4/HER4. therapeutic application,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10747938&form=6&db=m Activation of tumor necrosis factor-alpha-converting enzyme-mediated ectodomain shedding by nitric oxide. causal interaction,unassigned 4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10799546&form=6&db=m Stimulation-induced down-regulation of tumor necrosis factor-alpha converting enzyme. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10799547&form=6&db=m Functional analysis of the domain structure of tumor necrosis factor-alpha converting enzyme. diagnostic usage,ongoing research,therapeutic application,unassigned 2,1,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10801841&form=6&db=m Identification and characterization of human endometase (Matrix metalloproteinase-26) from endometrial tumor. ongoing research,unassigned 4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10849774&form=6&db=m Matrix metalloproteinases and TACE play a role in the pathogenesis of endometriosis. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11028485&form=6&db=m Expression of tumor necrosis factor-alpha--converting enzyme and tumor necrosis factor-alpha in human myocarditis. causal interaction,diagnostic usage,ongoing research,unassigned 3,4,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11083924&form=6&db=m Differential shedding of transmembrane neuregulin isoforms by the tumor necrosis factor-alpha-converting enzyme. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11108241&form=6&db=m Tumor necrosis factor-alpha converting enzyme (TACE) is a growth hormone binding protein (GHBP) sheddase: the metalloprotease TACE/ADAM-17 is critical for (PMA-induced) GH receptor proteolysis and GHBP generation. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11162616&form=6&db=m Full-length and N-TIMP-3 display equal inhibitory activities toward TNF-alpha convertase. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11238737&form=6&db=m Constitutive alpha-secretase cleavage of the beta-amyloid precursor protein in the furin-deficient LoVo cell line: involvement of the pro-hormone convertase 7 and the disintegrin metalloprotease ADAM10. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11254358&form=6&db=m Pulmonary hypoplasia in mice lacking tumor necrosis factor-alpha converting enzyme indicates an indispensable role for cell surface protein shedding during embryonic lung branching morphogenesis. ongoing research,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11278735&form=6&db=m Biochemical and pharmacological criteria define two shedding activities for TRANCE/OPGL that are distinct from the tumor necrosis factor alpha convertase. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11334139&form=6&db=m ADAM17 but not ADAM10 mediates tumor necrosis factor-alpha and L-selectin shedding from leukocyte membranes. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11375402&form=6&db=m Regulation of membrane metalloproteolytic cleavage of L-selectin (CD62l) by the epidermal growth factor domain. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11406201&form=6&db=m Up-regulation of TNF-alpha convertase (TACE/ADAM17) after oxygen-glucose deprivation in rat forebrain slices. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11460998&form=6&db=m Abrogation of tumor necrosis factor-alpha converting enzyme inhibits embryonic lung morphogenesis in culture. ongoing research,therapeutic application,unassigned 2,2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11463349&form=6&db=m Constitutive shedding of the amyloid precursor protein ectodomain is up-regulated by tumour necrosis factor-alpha converting enzyme. causal interaction,therapeutic application,unassigned 1,2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11477090&form=6&db=m The disintegrins ADAM10 and TACE contribute to the constitutive and phorbol ester-regulated normal cleavage of the cellular prion protein. therapeutic application,unassigned 4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11495925&form=6&db=m Tumor necrosis factor-alpha-converting enzyme (ADAM17) mediates the cleavage and shedding of fractalkine (CX3CL1). therapeutic application,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11571300&form=6&db=m Tumor necrosis factor-alpha-converting enzyme mediates the inducible cleavage of fractalkine. causal interaction,therapeutic application,unassigned 3,2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11576338&form=6&db=m A novel inhibitor of tumor necrosis factor-alpha converting enzyme ameliorates polycystic kidney disease. causal interaction,ongoing research,therapeutic application,unassigned 2,2,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11600492&form=6&db=m Metalloprotease-dependent protransforming growth factor-alpha ectodomain shedding in the absence of tumor necrosis factor-alpha-converting enzyme. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11677124&form=6&db=m Discovery of selective hydroxamic acid inhibitors of tumor necrosis factor-alpha converting enzyme. causal interaction,therapeutic application,unassigned 2,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11708926&form=6&db=m Design of selective and soluble inhibitors of tumor necrosis factor-alpha converting enzyme (TACE). therapeutic application,unassigned 4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11733179&form=6&db=m Tumor necrosis factor-alpha converting enzyme. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11782944&form=6&db=m Shedding light on sheddases: role in growth and development. therapeutic application,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11823465&form=6&db=m Tumor necrosis factor-alpha converting enzyme (TACE) regulates epidermal growth factor receptor ligand availability. diagnostic usage,ongoing research,unassigned 3,2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11857410&form=6&db=m Inhibition of metalloproteinases enhances the internalization of anti-CD30 antibody Ki-3 and the cytotoxic activity of Ki-3 immunotoxin. therapeutic application,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11878807&form=6&db=m A continuous fluorimetric assay for tumor necrosis factor-alpha converting enzyme. diagnostic usage,ongoing research,therapeutic application,unassigned 1,3,2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11884025&form=6&db=m Implication of TNF-alpha convertase (TACE/ADAM17) in inducible nitric oxide synthase expression and inflammation in an experimental model of colitis. causal interaction,ongoing research,therapeutic application,unassigned 4,2,2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12014967&form=6&db=m Beta-aryl-succinic acid hydroxamates as dual inhibitors of matrix metalloproteinases and tumor necrosis factor alpha converting enzyme. therapeutic application,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12015459&form=6&db=m Current concepts in the pathogenesis of meningitis caused by Streptococcus pneumoniae. causal interaction,therapeutic application,unassigned 3,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12044879&form=6&db=m The C-terminal domains of TACE weaken the inhibitory action of N-TIMP-3. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12057646&form=6&db=m Highly water-soluble matrix metalloproteinases inhibitors and their effects in a rat adjuvant-induced arthritis model. ongoing research,therapeutic application,unassigned 1,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12058067&form=6&db=m Extracellular signal-regulated kinase phosphorylates tumor necrosis factor alpha-converting enzyme at threonine 735: a potential role in regulated shedding. causal interaction,unassigned 4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12065742&form=6&db=m (E)-2(R)-[1(S)-(Hydroxycarbamoyl)-4-phenyl-3-butenyl]-2'-isobutyl-2'-(methanesulfonyl)-4-methylvalerohydrazide (Ro 32-7315), a selective and orally active inhibitor of tumor necrosis factor-alpha convertase. therapeutic application,unassigned 2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12135369&form=6&db=m The tumor necrosis factor-alpha converting enzyme (TACE): a unique metalloproteinase with highly defined substrate selectivity. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12147693&form=6&db=m Structure-function relationship and role of tumor necrosis factor-alpha-converting enzyme in the down-regulation of L-selectin by non-steroidal anti-inflammatory drugs. ongoing research,therapeutic application,unassigned 2,2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12208655&form=6&db=m Metalloproteinases and the modulation of GH signaling. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12403792&form=6&db=m Metalloprotease-mediated GH receptor proteolysis and GHBP shedding. Determination of extracellular domain stem region cleavage site. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12408705&form=6&db=m Discovery of gamma-lactam hydroxamic acids as selective inhibitors of tumor necrosis factor alpha converting enzyme: design, synthesis, and structure-activity relationships. therapeutic application,unassigned 4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12441351&form=6&db=m Tumor necrosis factor-alpha converting enzyme/ADAM 17 mediates MUC1 shedding. ongoing research,therapeutic application,unassigned 1,3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12447765&form=6&db=m Tumor necrosis factor-alpha-converting enzyme: its role in community-acquired pneumonia. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12472889&form=6&db=m Effect of tumor necrosis factor-alpha converting enzyme (TACE) and metalloprotease inhibitor on amyloid precursor protein metabolism in human neurons. ongoing research,therapeutic application,unassigned 3,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12527424&form=6&db=m Differential expression of plasminogen activator inhibitor-1, tumor necrosis factor-alpha, TNF-alpha converting enzyme and ADAMTS family members in murine fat territories. diagnostic usage,ongoing research,unassigned 1,3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12532790&form=6&db=m [The structural features and inhibitors of tumor necrosis factor-alpha converting enzyme] therapeutic application,unassigned 4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12551920&form=6&db=m Endoproteolysis of beta-secretase (beta-site amyloid precursor protein-cleaving enzyme) within its catalytic domain. A potential mechanism for regulation. causal interaction,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12556225&form=6&db=m Tailoring tissue inhibitor of metalloproteinases-3 to overcome the weakening effects of the cysteine-rich domains of tumour necrosis factor-alpha converting enzyme. ongoing research,therapeutic application,unassigned 2,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12590602&form=6&db=m Multiple metalloproteinases process protransforming growth factor-alpha (proTGF-alpha). causal interaction,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12606576&form=6&db=m TACE is required for the activation of the EGFR by TGF-alpha in tumors. causal interaction,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12621058&form=6&db=m Characterization of growth factor-induced serine phosphorylation of tumor necrosis factor-alpha converting enzyme and of an alternatively translated polypeptide. ongoing research,unassigned 2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12629177&form=6&db=m Glycoprotein 130 signaling regulates Notch1 expression and activation in the self-renewal of mammalian forebrain neural stem cells. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12668732&form=6&db=m Identification of SAP97 as an intracellular binding partner of TACE. causal interaction,unassigned 4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12670535&form=6&db=m Identification of a selectivity determinant for inhibition of tumor necrosis factor-alpha converting enzyme by comparative modeling. causal interaction,diagnostic usage,therapeutic application,unassigned 3,3,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12706122&form=6&db=m Intracellular maturation and transport of tumor necrosis factor alpha converting enzyme. ongoing research,therapeutic application,unassigned 2,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12711607&form=6&db=m Tobacco smoke-induced lung cell proliferation mediated by tumor necrosis factor alpha-converting enzyme and amphiregulin. ongoing research,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12714508&form=6&db=m The disintegrin-like metalloproteinase ADAM10 is involved in constitutive cleavage of CX3CL1 (fractalkine) and regulates CX3CL1-mediated cell-cell adhesion. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12714588&form=6&db=m Impaired trafficking and activation of tumor necrosis factor-alpha-converting enzyme in cell mutants defective in protein ectodomain shedding. causal interaction,ongoing research,unassigned 3,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12723945&form=6&db=m Design, synthesis, and evaluation of benzothiadiazepine hydroxamates as selective tumor necrosis factor-alpha converting enzyme inhibitors. therapeutic application,unassigned 4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12755693&form=6&db=m Tumor necrosis factor-alpha converting enzyme is processed by proprotein-convertases to its mature form which is degraded upon phorbol ester stimulation. ongoing research,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12773386&form=6&db=m Defective valvulogenesis in HB-EGF and TACE-null mice is associated with aberrant BMP signaling. ongoing research,unassigned 2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12781187&form=6&db=m Discovery of selective phosphonamide-based inhibitors of tumor necrosis factor-alpha converting enzyme (TACE). causal interaction,therapeutic application,unassigned 2,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12781190&form=6&db=m Discovery of N-hydroxy-2-(2-oxo-3-pyrrolidinyl)acetamides as potent and selective inhibitors of tumor necrosis factor-alpha converting enzyme (TACE). therapeutic application,unassigned 4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12789686&form=6&db=m Protease inhibitors of the sulfonamide type: anticancer, antiinflammatory, and antiviral agents. causal interaction,therapeutic application,unassigned 4,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12810728&form=6&db=m Membrane-anchored CD40 is processed by the tumor necrosis factor-alpha-converting enzyme. Implications for CD40 signaling. ongoing research,therapeutic application,unassigned 3,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12814936&form=6&db=m TACE/ADAM17 processing of EGFR ligands indicates a role as a physiological convertase. ongoing research,unassigned 2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12814963&form=6&db=m CYP3A induction by N-hydroxyformamide tumor necrosis factor-alpha converting enzyme/matrix metalloproteinase inhibitors use of a pregname X receptor activation assay and primary hepatocyte culture for assessing induction potential in humans. therapeutic application,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12869563&form=6&db=m Ectodomain cleavage of ErbB-4: characterization of the cleavage site and m80 fragment. ongoing research,therapeutic application,unassigned 1,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12878595&form=6&db=m Stimulated shedding of vascular cell adhesion molecule 1 (VCAM-1) is mediated by tumor necrosis factor-alpha-converting enzyme (ADAM 17). causal interaction,ongoing research,unassigned 1,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12901873&form=6&db=m TACE/ADAM-17 enzymatic activity is increased in response to cellular stimulation. ongoing research,unassigned 2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12912811&form=6&db=m Targeted overexpression of transmembrane tumor necrosis factor provokes a concentric cardiac hypertrophic phenotype. therapeutic application,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12941954&form=6&db=m Phorbol 12-myristate 13-acetate-induced ectodomain shedding and phosphorylation of the human meprinbeta metalloprotease. causal interaction,therapeutic application,unassigned 2,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12949242&form=6&db=m ADAM-17-independent shedding of L-selectin. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12972643&form=6&db=m Tumor necrosis factor alpha-converting enzyme mediates MUC5AC mucin expression in cultured human airway epithelial cells. causal interaction,ongoing research,unassigned 1,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=14499647&form=6&db=m TACE is required for fetal murine cardiac development and modeling. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=14515145&form=6&db=m Structure and functions of tumor necrosis factor-alpha converting enzyme. therapeutic application,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=14532978&form=6&db=m Expression of ADAMs (a disintegrin and metalloproteases) and TIMP-3 (tissue inhibitor of metalloproteinase-3) in human prostatic adenocarcinomas. causal interaction,diagnostic usage,ongoing research,unassigned 3,1,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=14567681&form=6&db=m Drosophila TIMP is a potent inhibitor of MMPs and TACE: similarities in structure and function to TIMP-3. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=14579524&form=6&db=m Design strategies for the identification of MMP-13 and Tace inhibitors. causal interaction,therapeutic application,unassigned 4,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=14587283&form=6&db=m Role of TIMPs (tissue inhibitors of metalloproteinases) in pericellular proteolysis: the specificity is in the detail. causal interaction,unassigned 4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=14623079&form=6&db=m TACE/ADAM-17 maturation and activation of sheddase activity require proprotein convertase activity. causal interaction,therapeutic application,unassigned 1,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=14625290&form=6&db=m Tumor necrosis factor-alpha-converting enzyme controls surface expression of c-Kit and survival of embryonic stem cell-derived mast cells. causal interaction,diagnostic usage,ongoing research,therapeutic application 2,3,2,1 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=14638693&form=6&db=m Evidence for a critical role of the tumor necrosis factor alpha convertase (TACE) in ectodomain shedding of the p75 neurotrophin receptor (p75NTR). ongoing research,unassigned 4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=14678276&form=6&db=m Tumour necrosis factor-alpha converting enzyme (TACE) activity in human colonic epithelial cells. causal interaction,ongoing research,unassigned 1,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=14699008&form=6&db=m Targeted overexpression of noncleavable and secreted forms of tumor necrosis factor provokes disparate cardiac phenotypes. causal interaction,therapeutic application,unassigned 3,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=14751236&form=6&db=m Inactivating mutations block the tumor necrosis factor-alpha-converting enzyme in the early secretory pathway. causal interaction,unassigned 4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=14987279&form=6&db=m Localization of tumour necrosis factor-alpha converting enzyme in normal human skin. ongoing research,unassigned 4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15026328&form=6&db=m Cannabinoids induce cancer cell proliferation via tumor necrosis factor alpha-converting enzyme (TACE/ADAM17)-mediated transactivation of the epidermal growth factor receptor. ongoing research,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15044618&form=6&db=m Inhibition of tumor necrosis factor-alpha-converting enzyme by a selective antagonist protects brain from focal ischemic injury in rats. causal interaction,unassigned 4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15066986&form=6&db=m Selective roles for tumor necrosis factor alpha-converting enzyme/ADAM17 in the shedding of the epidermal growth factor receptor ligand family: the juxtamembrane stalk determines cleavage efficiency. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15066987&form=6&db=m A cellular metalloproteinase activates Vibrio cholerae pro-cytolysin. diagnostic usage,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15075334&form=6&db=m Loss of ectodomain shedding due to mutations in the metalloprotease and cysteine-rich/disintegrin domains of the tumor necrosis factor-alpha converting enzyme (TACE). unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15100227&form=6&db=m Inhibition of the tumor necrosis factor-alpha-converting enzyme by its pro domain. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15102849&form=6&db=m Pronounced diversity in electronic and chemical properties between the catalytic zinc sites of tumor necrosis factor-alpha-converting enzyme and matrix metalloproteinases despite their high structural similarity. ongoing research,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15103332&form=6&db=m Ectodomain shedding of the glycoprotein GP of Ebola virus. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15121636&form=6&db=m Cigarette smoke induces MUC5AC mucin overproduction via tumor necrosis factor-alpha-converting enzyme in human airway epithelial (NCI-H292) cells. ongoing research,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15130087&form=6&db=m MT1-MMP mediates MUC1 shedding independent of TACE/ADAM17. ongoing research,unassigned 2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15182369&form=6&db=m The role of ADAM10 and ADAM17 in the ectodomain shedding of angiotensin converting enzyme and the amyloid precursor protein. ongoing research,unassigned 4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15197174&form=6&db=m Cell-matrix interaction via CD44 is independently regulated by different metalloproteinases activated in response to extracellular Ca(2+) influx and PKC activation. ongoing research,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15206946&form=6&db=m Tumour necrosis factor-alpha stimulates expression of TNF-alpha converting enzyme in endothelial cells. causal interaction,ongoing research,unassigned 2,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15215246&form=6&db=m Natural soluble interleukin-15Ralpha is generated by cleavage that involves the tumor necrosis factor-alpha-converting enzyme (TACE/ADAM17). unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15308656&form=6&db=m Delineating the molecular basis of the inactivity of tissue inhibitor of metalloproteinase-2 against tumor necrosis factor-alpha-converting enzyme. therapeutic application,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15309730&form=6&db=m ADAM17 mRNA expression and pathological features of hepatocellular carcinoma. causal interaction,diagnostic usage,ongoing research,unassigned 1,4,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15319441&form=6&db=m Metalloproteinases and transforming growth factor-alpha mediate substance P-induced mitogen-activated protein kinase activation and proliferation in human colonocytes. causal interaction,ongoing research,therapeutic application,unassigned 3,2,3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15337756&form=6&db=m Distinct ADAM metalloproteinases regulate G protein-coupled receptor-induced cell proliferation and survival. causal interaction,ongoing research,unassigned 1,3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15345652&form=6&db=m Tumor necrosis factor-alpha-converting enzyme (ADAM17) mediates GPIbalpha shedding from platelets in vitro and in vivo. ongoing research,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15531300&form=6&db=m Characterization of (2R, 3S)-2-([[4-(2-butynyloxy)phenyl]sulfonyl]amino)-N,3-dihydroxybutanamide, a potent and selective inhibitor of TNF-alpha converting enzyme. causal interaction,therapeutic application,unassigned 3,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15556048&form=6&db=m Increased expression of tumor necrosis factor-alpha converting enzyme and tumor necrosis factor-alpha in peripheral blood mononuclear cells in patients with advanced congestive heart failure. causal interaction,diagnostic usage,ongoing research,unassigned 3,3,3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15566296&form=6&db=m Synthesis and structure-activity relationships of 4-alkynyloxy phenyl sulfanyl, sulfinyl, and sulfonyl alkyl hydroxamates as tumor necrosis factor-alpha converting enzyme and matrix metalloproteinase inhibitors. therapeutic application,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15591071&form=6&db=m Oxidation of cholesterol by amyloid precursor protein and beta-amyloid peptide. ongoing research,unassigned 4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15641051&form=6&db=m Interleukin-6 receptor shedding is enhanced by interleukin-1beta and tumor necrosis factor alpha and is partially mediated by tumor necrosis factor alpha-converting enzyme in osteoblast-like cells. causal interaction,unassigned 4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15647744&form=6&db=m TNFR1 upregulation mediates tolerance after brain ischemic preconditioning. causal interaction,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15713681&form=6&db=m Total conversion of tissue inhibitor of metalloproteinase (TIMP) for specific metalloproteinase targeting: fine-tuning TIMP-4 for optimal inhibition of tumor necrosis factor-{alpha}-converting enzyme. therapeutic application,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15739225&form=6&db=m Developmental expression of metalloproteases ADAM 9, 10, and 17 becomes restricted to divergent pancreatic compartments. causal interaction,diagnostic usage,ongoing research,unassigned 4,3,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15743767&form=6&db=m Growth hormone receptor is a target for presenilin-dependent gamma-secretase cleavage. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15746097&form=6&db=m Presenilin-dependent gamma-secretase processing regulates multiple ERBB4/HER4 activities. therapeutic application,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15774823&form=6&db=m Transforming growth factor alpha (TGF-alpha) and other targets of tumor necrosis factor-alpha converting enzyme (TACE) in murine polycystic kidney disease. causal interaction,diagnostic usage,ongoing research,therapeutic application 2,3,1,1 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15784625&form=6&db=m Nectin-4, a new serological breast cancer marker, is a substrate for tumor necrosis factor-alpha-converting enzyme (TACE)/ADAM-17. causal interaction,therapeutic application,unassigned 2,3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15801829&form=6&db=m A comparison of the binding sites of matrix metalloproteinases and tumor necrosis factor-alpha converting enzyme: implications for selectivity. therapeutic application,unassigned 2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15836657&form=6&db=m Severity of coronary artery stenosis is associated with a polymorphism in the CXCL16/SR-PSOX gene. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15857301&form=6&db=m Therapeutic potential of TACE inhibitors in stroke. causal interaction,therapeutic application,unassigned 2,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15859325&form=6&db=m [Screening of TACE peptide inhibitors from a phage display random 15-peptide library by recombinant TACE ecotodomain] causal interaction,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15908214&form=6&db=m Non-hydroxamate 5-phenylpyrimidine-2,4,6-trione derivatives as selective inhibitors of tumor necrosis factor-alpha converting enzyme. causal interaction,therapeutic application,unassigned 2,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15923650&form=6&db=m ERK-mediated phosphorylation of Thr735 in TNFalpha-converting enzyme and its potential role in TACE protein trafficking. causal interaction,unassigned 2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15942356&form=6&db=m Regulation of peritoneal and systemic neutrophil-derived tumor necrosis factor-alpha release in patients with severe peritonitis: role of tumor necrosis factor-alpha converting enzyme cleavage. ongoing research,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15942388&form=6&db=m Caught in the act: observation of polymorphonuclear neutrophils for the regulation of tumor necrosis factor-alpha release by tumor necrosis factor-alpha converting enzyme in patients with secondary peritonitis. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16020548&form=6&db=m Shedding of collagen XVII ectodomain depends on plasma membrane microenvironment. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16037568&form=6&db=m Combination of tumor necrosis factor-alpha ablation and matrix metalloproteinase inhibition prevents heart failure after pressure overload in tissue inhibitor of metalloproteinase-3 knock-out mice. causal interaction,ongoing research,therapeutic application,unassigned 3,3,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16041691&form=6&db=m Up-regulated expression of ADAM17 in human colon carcinoma: co-expression with EGFR in neoplastic and endothelial cells. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,4,1 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16079149&form=6&db=m Reactive site mutations in tissue inhibitor of metalloproteinase-3 disrupt inhibition of matrix metalloproteinases but not tumor necrosis factor-alpha-converting enzyme. causal interaction,therapeutic application,unassigned 1,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16127421&form=6&db=m Continuous real-time measurement of tumor necrosis factor-alpha converting enzyme activity on live cells. ongoing research,unassigned 4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16134057&form=6&db=m Expression of TNFalpha and its receptors R1 and R2 in human alveolar epithelial cells exposed to organic dust and the effects of 8-bromo-cAMP and protein kinase A modulation. diagnostic usage,ongoing research,unassigned 3,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16177050&form=6&db=m Green tea epigallocatechin-3-gallate (EGCG) modulates amyloid precursor protein cleavage and reduces cerebral amyloidosis in Alzheimer transgenic mice. diagnostic usage,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16183650&form=6&db=m Phorbol ester-induced apoptosis in prostate cancer cells via autocrine activation of the extrinsic apoptotic cascade: a key role for protein kinase C delta. causal interaction,ongoing research,therapeutic application,unassigned 4,3,2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16221290&form=6&db=m Tumor necrosis factor-alpha-converting enzyme is expressed in the inflamed peripheral nervous system. causal interaction,unassigned 4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16221845&form=6&db=m NMDA receptor activation inhibits alpha-secretase and promotes neuronal amyloid-beta production. causal interaction,unassigned 4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16236709&form=6&db=m The disintegrin ADAM9 indirectly contributes to the physiological processing of cellular prion by modulating ADAM10 activity. causal interaction,therapeutic application,unassigned 1,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16251361&form=6&db=m Proteolytic cleavage and phosphorylation of a tumor-associated ErbB4 isoform promote ligand-independent survival and cancer cell growth. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,3,4,2 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16273118&form=6&db=m Human colonic myocytes are involved in postischemic inflammation through ADAM17-dependent TNFalpha production. ongoing research,therapeutic application,unassigned 1,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16298020&form=6&db=m 15,16-dihydrotanshinone I suppresses the activation of BV-2 cell, a murine microglia cell line, by lipopolysaccharide. ongoing research,unassigned 2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16332693&form=6&db=m Tumor necrosis factor-alpha-converting enzyme (TACE/ADAM-17) mediates the ectodomain cleavage of intercellular adhesion molecule-1 (ICAM-1). ongoing research,therapeutic application,unassigned 3,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16336275&form=6&db=m Human airway trypsin-like protease induces amphiregulin release through a mechanism involving protease-activated receptor-2-mediated ERK activation and TNF alpha-converting enzyme activity in airway epithelial cells. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16376986&form=6&db=m Tumour necrosis factor-alpha converting enzyme in human gestational tissues from pregnancies complicated by chorioamnionitis. causal interaction,ongoing research,unassigned 3,2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16378499&form=6&db=m Inhibitors of TACE and Caspase-1 as anti-inflammatory drugs. causal interaction,therapeutic application,unassigned 1,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16393139&form=6&db=m Tumour necrosis factor alpha-converting enzyme mediates ectodomain shedding of Vps10p-domain receptor family members. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16399672&form=6&db=m Hypothalamic tumor necrosis factor-alpha converting enzyme mediates excitatory amino acid-dependent neuron-to-glia signaling in the neuroendocrine brain. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16463648&form=6&db=m Screening of TACE peptide inhibitors from phage display peptide library. therapeutic application,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16497166&form=6&db=m Modulation of autocrine TNF-alpha-stimulated matrix metalloproteinase 9 (MMP-9) expression by mitogen-activated protein kinases in THP-1 monocytic cells. causal interaction,ongoing research,therapeutic application,unassigned 4,1,3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16679521&form=6&db=m The TACE zymogen: re-examining the role of the cysteine switch. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16735599&form=6&db=m ADAM17 deficiency by mature neutrophils has differential effects on L-selectin shedding. causal interaction,unassigned 2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16737974&form=6&db=m 5-HT2A receptor induces ERK phosphorylation and proliferation through ADAM-17 tumor necrosis factor-alpha-converting enzyme (TACE) activation and heparin-bound epidermal growth factor-like growth factor (HB-EGF) shedding in mesangial cells. causal interaction,ongoing research,unassigned 1,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16782893&form=6&db=m Proteomic identification of desmoglein 2 and activated leukocyte cell adhesion molecule as substrates of ADAM17 and ADAM10 by difference gel electrophoresis. causal interaction,therapeutic application,unassigned 4,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16790761&form=6&db=m Doxycycline reduces mortality and injury to the brain and cochlea in experimental pneumococcal meningitis. causal interaction,unassigned 4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16799629&form=6&db=m Differential regulation of tumor necrosis factor-alpha-converting enzyme and angiotensin-converting enzyme by type I and II interferons in human normal and leukemic myeloid cells. causal interaction,ongoing research,unassigned 4,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16806998&form=6&db=m High molecular weight hyaluronic acid down-regulates the gene expression of osteoarthritis-associated cytokines and enzymes in fibroblast-like synoviocytes from patients with early osteoarthritis. ongoing research,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16809777&form=6&db=m Ectodomain shedding of preadipocyte factor 1 (Pref-1) by tumor necrosis factor alpha converting enzyme (TACE) and inhibition of adipocyte differentiation. therapeutic application,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16900751&form=6&db=m Upregulation of ADAM-17 expression in active lesions in multiple sclerosis. causal interaction,ongoing research,unassigned 4,3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16909010&form=6&db=m APP processing and the APP-KPI domain involvement in the amyloid cascade. diagnostic usage,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16912185&form=6&db=m Multiple Acquired Renal Carcinoma Tumor Capabilities Abolished upon Silencing of ADAM17. causal interaction,ongoing research,unassigned 3,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16923819&form=6&db=m Nardilysin enhances ectodomain shedding of heparin-binding epidermal growth factor-like growth factor through activation of tumor necrosis factor-alpha-converting enzyme. causal interaction,unassigned 2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16926839&form=6&db=m Stroke-induced subventricular zone proliferation is promoted by tumor necrosis factor-alpha-converting enzyme protease activity. ongoing research,therapeutic application,unassigned 2,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16988945&form=6&db=m Impact of IGF-1R/EGFR cross-talks on hepatoma cell sensitivity to gefitinib. causal interaction,diagnostic usage,unassigned 1,3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17026478&form=6&db=m Effect of pro-inflammatory stimuli on mucin expression and inhibition by secretory leucoprotease inhibitor. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17027261&form=6&db=m Discovery of low nanomolar non-hydroxamate inhibitors of tumor necrosis factor-alpha converting enzyme (TACE). causal interaction,therapeutic application,unassigned 1,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17027649&form=6&db=m ErbB-4 and TNF-alpha converting enzyme localization to membrane microdomains. ongoing research,therapeutic application,unassigned 1,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17047157&form=6&db=m A soluble form of the Mer receptor tyrosine kinase inhibits macrophage clearance of apoptotic cells and platelet aggregation. therapeutic application,unassigned 4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17060126&form=6&db=m Blockade of tumor necrosis factor-alpha-converting enzyme improves experimental small intestinal damage by decreasing matrix metalloproteinase-3 production in rats. ongoing research,therapeutic application,unassigned 2,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17116701&form=6&db=m Pref-1, a preadipocyte secreted factor that inhibits adipogenesis. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17164725&form=6&db=m TIMP-3 ameliorates hepatic ischemia/reperfusion injury through inhibition of tumor necrosis factor-alpha-converting enzyme activity in rats. causal interaction,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17169360&form=6&db=m Ectodomain shedding of the EGF-receptor ligand epigen is mediated by ADAM17. causal interaction,therapeutic application,unassigned 3,3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17169570&form=6&db=m Expression and protein chemistry yielding crystallization of the catalytic domain of ADAM17 complexed with a hydroxamate inhibitor. therapeutic application,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17172985&form=6&db=m Nonischemic lung injury by mediators from unilateral ischemic reperfused lung: ameliorating effect of tumor necrosis factor-alpha-converting enzyme inhibitor. causal interaction,ongoing research,unassigned 2,2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17178880&form=6&db=m Cross-talk between G protein-coupled receptor and epidermal growth factor receptor signaling pathways contributes to growth and invasion of head and neck squamous cell carcinoma. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,3,2 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17180679&form=6&db=m ADAM-17 associated with CD44 cleavage and metastasis in oral squamous cell carcinoma. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,2,4,1 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17188863&form=6&db=m Discovery of novel hydantoins as selective non-hydroxamate inhibitors of tumor necrosis factor-alpha converting enzyme (TACE). causal interaction,therapeutic application,unassigned 3,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17218812&form=6&db=m Innate immune mucin production via epithelial cell surface signaling: relationship to allergic disease. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17220369&form=6&db=m Regulation of interleukin-8 via an airway epithelial signaling cascade. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17227756&form=6&db=m Post-transcriptional up-regulation of ADAM17 upon epidermal growth factor receptor activation and in breast tumors. causal interaction,diagnostic usage,ongoing research,unassigned 3,2,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17283047&form=6&db=m Mitogenic activity and signaling mechanism of 2-(14,15- epoxyeicosatrienoyl)glycerol, a novel cytochrome p450 arachidonate metabolite. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17303576&form=6&db=m Hypoxia-inducible factor 1alpha (HIF-1alpha)-mediated hypoxia increases BACE1 expression and beta-amyloid generation. causal interaction,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17327231&form=6&db=m Soluble Interleukin IL-15Ralpha is generated by alternative splicing or proteolytic cleavage and forms functional complexes with IL-15. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17332143&form=6&db=m Effect of DPC 333 [(2R)-2-{(3R)-3-amino-3-[4-(2-methylquinolin-4-ylmethoxy)phenyl]-2-oxopyrrolidin-1-yl}-N-hydroxy-4-methylpentanamide], a human tumor necrosis factor alpha-converting enzyme inhibitor, on the disposition of methotrexate: a transporter-based drug-drug interaction case study. causal interaction,ongoing research,therapeutic application,unassigned 2,2,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17352738&form=6&db=m Meltrin beta (ADAM19) mediates ectodomain shedding of Neuregulin beta1 in the Golgi apparatus: fluorescence correlation spectroscopic observation of the dynamics of ectodomain shedding in living cells. causal interaction,therapeutic application,unassigned 3,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17355261&form=6&db=m Inhibition of ADAM17 reduces hypoxia-induced brain tumor cell invasiveness. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,4,4 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17355265&form=6&db=m ADAMs in cancer cell proliferation and progression. causal interaction,unassigned 2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17357475&form=6&db=m Comparison of properties of tumor necrosis factor-alpha converting enzyme (TACE) and some matrix metalloproteases (MMPs) in catalytic domains. ongoing research,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17360351&form=6&db=m Key feature of the catalytic cycle of TNF-alpha converting enzyme involves communication between distal protein sites and the enzyme catalytic core. ongoing research,therapeutic application,unassigned 2,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17368021&form=6&db=m Hydantoins, triazolones, and imidazolones as selective non-hydroxamate inhibitors of tumor necrosis factor-alpha converting enzyme (TACE). therapeutic application,unassigned 4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17433308&form=6&db=m Shedding of the p75NTR neurotrophin receptor is modulated by lipid rafts. causal interaction,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17438092&form=6&db=m ADAM-17 expression in breast cancer correlates with variables of tumor progression. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,4,2 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17464354&form=6&db=m Substitution of methionine 435 with leucine, isoleucine, and serine in tumor necrosis factor alpha converting enzyme inactivates ectodomain shedding activity. causal interaction,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17545155&form=6&db=m Extracellular phosphorylation of collagen XVII by ecto-casein kinase 2 inhibits ectodomain shedding. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17546624&form=6&db=m Interleukin-4 antagonizes oncostatin M and transforming growth factor beta-induced responses in articular chondrocytes. causal interaction,therapeutic application,unassigned 3,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17572069&form=6&db=m Cyclooxygenase-2 transactivates the epidermal growth factor receptor through specific E-prostanoid receptors and tumor necrosis factor-alpha converting enzyme. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,2,1 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17608729&form=6&db=m TACE: a new target in epidermal growth factor receptor dependent tumors. causal interaction,ongoing research,therapeutic application,unassigned 4,1,3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17646208&form=6&db=m Mice heterozygous for tumor necrosis factor-alpha converting enzyme are protected from obesity-induced insulin resistance and diabetes. ongoing research,therapeutic application,unassigned 3,2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17656469&form=6&db=m Pharmacokinetics and pharmacodynamics of DPC 333 ((2R)-2-((3R)-3-amino-3{4-[2-methyl-4-quinolinyl) methoxy] phenyl}-2-oxopyrrolidinyl)-N-hydroxy-4-methylpentanamide)), a potent and selective inhibitor of tumor necrosis factor alpha-converting enzyme in rodents, dogs, chimpanzees, and humans. therapeutic application,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17822026&form=6&db=m [Inhibition of proliferation, adhesion and invasion ability of human lung carcinoma cell A549 by tumor necrosis factor-alpha converting enzyme (TACE)] ongoing research,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17884817&form=6&db=m Hypoxia-inducible factor mediates hypoxic and tumor necrosis factor alpha-induced increases in tumor necrosis factor-alpha converting enzyme/ADAM17 expression by synovial cells. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17895248&form=6&db=m The ADAM10 prodomain is a specific inhibitor of ADAM10 proteolytic activity and inhibits cellular shedding events. causal interaction,therapeutic application,unassigned 3,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17945434&form=6&db=m Huperzine A regulates amyloid precursor protein processing via protein kinase C and mitogen-activated protein kinase pathways in neuroblastoma SK-N-SH cells over-expressing wild type human amyloid precursor protein 695. causal interaction,ongoing research,therapeutic application,unassigned 3,4,3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17963710&form=6&db=m Application of structural dynamic approaches provide novel insights into the enzymatic mechanism of the tumor necrosis factor-alpha-converting enzyme. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17999917&form=6&db=m Involvement of NF-kappaB-mediated maturation of ADAM-17 in the invasion of oral squamous cell carcinoma. causal interaction,ongoing research,unassigned 3,3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18040288&form=6&db=m The transmembrane domain of TACE regulates protein ectodomain shedding. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18234496&form=6&db=m Alpha,Beta-cyclic-beta-benzamido hydroxamic acids: Novel oxaspiro[4.4]nonane templates for the discovery of potent, selective, orally bioavailable inhibitors of tumor necrosis factor-alpha converting enzyme (TACE). therapeutic application,unassigned 4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18238782&form=6&db=m ADAM-17 predicts adverse outcome in patients with breast cancer. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,4,3 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18239612&form=6&db=m Production of the soluble form of KIT, s-KIT, abolishes stem cell factor-induced melanogenesis in human melanocytes. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18247549&form=6&db=m Discovery of novel hydroxamates as highly potent tumor necrosis factor-alpha converting enzyme inhibitors: part I--discovery of two binding modes. diagnostic usage,therapeutic application,unassigned 3,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18276953&form=6&db=m Tumor necrosis factor-alpha converting enzyme in the human placenta throughout gestation. causal interaction,ongoing research,therapeutic application,unassigned 3,3,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18282708&form=6&db=m Potent, selective, orally bioavailable inhibitors of tumor necrosis factor-alpha converting enzyme (TACE): discovery of indole, benzofuran, imidazopyridine and pyrazolopyridine P1' substituents. therapeutic application,unassigned 4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18284555&form=6&db=m 3D-quantitative structure-activity relationship studies on benzothiadiazepine hydroxamates as inhibitors of tumor necrosis factor-alpha converting enzyme. diagnostic usage,ongoing research,therapeutic application,unassigned 3,3,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18296613&form=6&db=m Tumor necrosis factor-alpha-converting enzyme (TACE) levels in periodontal diseases. diagnostic usage,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18322947&form=6&db=m Expression of tumor necrosis factor-alpha converting enzyme in liver regeneration after partial hepatectomy. diagnostic usage,ongoing research,unassigned 1,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18367087&form=6&db=m mGluR1/5-dependent long-term depression requires the regulated ectodomain cleavage of neuronal pentraxin NPR by TACE. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18390808&form=6&db=m p38 mitogen-activated protein kinase-dependent tumor necrosis factor-alpha-converting enzyme is important for liver injury in hepatotoxic interaction between lipopolysaccharide and ranitidine. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18426733&form=6&db=m Expression of tumor necrosis factor alpha converting enzyme in endocrine cancers. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,3,2,1 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18436796&form=6&db=m Heparin-binding epidermal growth factor-like growth factor signaling in flow-induced arterial remodeling. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18483276&form=6&db=m The soluble alpha chain of interleukin-15 receptor: a proinflammatory molecule associated with tumor progression in head and neck cancer. causal interaction,diagnostic usage,ongoing research,unassigned 1,2,2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18600307&form=6&db=m Polymorphisms of the tumor necrosis factor-alpha (TNF) and the TNF-alpha converting enzyme (TACE/ADAM17) genes in relation to cardiovascular mortality: the AtheroGene study. ongoing research,therapeutic application,unassigned 1,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18621108&form=6&db=m Diverse roles of matrix metalloproteinases and tissue inhibitors of metalloproteinases in neuroinflammation and cerebral ischemia. causal interaction,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18676862&form=6&db=m Tumor-associated MICA is shed by ADAM proteases. causal interaction,therapeutic application,unassigned 1,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18690780&form=6&db=m Metastasis-associated C4.4A, a GPI-anchored protein cleaved by ADAM10 and ADAM17. causal interaction,ongoing research,therapeutic application,unassigned 3,3,3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18713734&form=6&db=m Metalloproteinase- and gamma-secretase-mediated cleavage of protein-tyrosine phosphatase receptor type Z. ongoing research,unassigned 2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18718504&form=6&db=m Neuronal RA175/SynCAM1 isoforms are processed by tumor necrosis factor-alpha-converting enzyme (TACE)/ADAM17-like proteases. causal interaction,therapeutic application,unassigned 4,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18762577&form=6&db=m TLR ligand-induced podosome disassembly in dendritic cells is ADAM17 dependent. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18772236&form=6&db=m Aldose reductase regulates high glucose-induced ectodomain shedding of tumor necrosis factor (TNF)-alpha via protein kinase C-delta and TNF-alpha converting enzyme in vascular smooth muscle cells. ongoing research,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18818406&form=6&db=m VEGF-A stimulates ADAM17-dependent shedding of VEGFR2 and crosstalk between VEGFR2 and ERK signaling. therapeutic application,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18835710&form=6&db=m Discovery of novel hydroxamates as highly potent tumor necrosis factor-alpha converting enzyme inhibitors. Part II: Optimization of the S3' pocket. therapeutic application,unassigned 4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18922903&form=6&db=m Src and ADAM-17-mediated shedding of transforming growth factor-alpha is a mechanism of acute resistance to TRAIL. causal interaction,ongoing research,therapeutic application,unassigned 2,4,2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18951988&form=6&db=m The good, the bad and the ugly substrates for ADAM10 and ADAM17 in brain pathology, inflammation and cancer. therapeutic application,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18971959&form=6&db=m ADAM10 is the constitutive functional sheddase of CD44 in human melanoma cells. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,3,4,1 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18979631&form=6&db=m Metastasis-associated C4.4A, a GPI-anchored protein cleaved by ADAM10 and ADAM17. causal interaction,ongoing research,therapeutic application,unassigned 3,3,3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18991041&form=6&db=m Upregulation of tumor necrosis factor receptor 1 and TNF-alpha converting enzyme during corneal wound healing. causal interaction,therapeutic application,unassigned 3,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19027012&form=6&db=m Tissue inhibitor of metalloproteinase 3 deficiency causes hepatic steatosis and adipose tissue inflammation in mice. causal interaction,therapeutic application,unassigned 3,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19066089&form=6&db=m Tissue inhibitor of matrix metalloproteinases-3 (TIMP-3) lacks involvement in bacterial collagenase-induced intracerebral hemorrhage in mouse. ongoing research,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19107625&form=6&db=m Chlorella powder inhibits the activities of peptidase cathepsin S, PLA2, cyclooxygenase-2, thromboxane synthase, tyrosine phosphatases, tumor necrosis factor-alpha converting enzyme, calpain and kinases. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19111539&form=6&db=m TIMP-3 and MMP-3 contribute to delayed inflammation and hippocampal neuronal death following global ischemia. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19147560&form=6&db=m Transforming growth factor beta induces clustering of HER2 and integrins by activating Src-focal adhesion kinase and receptor association to the cytoskeleton. causal interaction,therapeutic application,unassigned 3,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19152638&form=6&db=m Development of predictive 3D-QSAR CoMFA and CoMSIA models for beta-aminohydroxamic acid-derived tumor necrosis factor-alpha converting enzyme inhibitors. diagnostic usage,ongoing research,therapeutic application,unassigned 3,3,3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19171023&form=6&db=m Removal of cell surface heparan sulfate increases TACE activity and cleavage of ErbB4 receptor. causal interaction,ongoing research,therapeutic application,unassigned 4,1,3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19190330&form=6&db=m Human renal cancer cells express a novel membrane-bound interleukin-15 that induces, in response to the soluble interleukin-15 receptor alpha chain, epithelial-to-mesenchymal transition. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19218331&form=6&db=m Bisphenol A disrupts Notch signaling by inhibiting gamma-secretase activity and causes eye dysplasia of Xenopus laevis. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19223914&form=6&db=m Niaspan treatment increases tumor necrosis factor-alpha-converting enzyme and promotes arteriogenesis after stroke. ongoing research,therapeutic application,unassigned 1,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19228719&form=6&db=m Role of ADAMs in cancer formation and progression. causal interaction,therapeutic application,unassigned 3,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19239642&form=6&db=m Porphyromonas gingivalis stimulates TACE production by T cells. therapeutic application,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19276374&form=6&db=m Identification of ligand-induced proteolytic cleavage and ectodomain shedding of VEGFR-1/FLT1 in leukemic cancer cells. causal interaction,ongoing research,therapeutic application,unassigned 3,3,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19296470&form=6&db=m MicroRNA-122, a tumor suppressor microRNA that regulates intrahepatic metastasis of hepatocellular carcinoma. causal interaction,diagnostic usage,therapeutic application,unassigned 4,1,3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19298600&form=6&db=m Up-regulated expression of ADAM17 in gastrointestinal stromal tumors: coexpression with EGFR and EGFR ligands. causal interaction,diagnostic usage,ongoing research,unassigned 4,3,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19376560&form=6&db=m In situ evidence of involvement of Schwann cells in ulcerative colitis: autocrine and paracrine signaling by A disintegrin and metalloprotease-17-mediated tumor necrosis factor alpha production. causal interaction,diagnostic usage,ongoing research,unassigned 4,3,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19380613&form=6&db=m Soluble Form of the (Pro)Renin Receptor Generated by Intracellular Cleavage by Furin Is Secreted in Plasma. ongoing research,therapeutic application,unassigned 1,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19407014&form=6&db=m Release of soluble tumor necrosis factor receptor 1 from corneal epithelium by TNF-alpha converting enzyme dependent ectodomain shedding. ongoing research,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19408347&form=6&db=m The role of ADAMs in disease pathophysiology. causal interaction,therapeutic application,unassigned 3,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19426283&form=6&db=m Serotonin stimulates platelet receptor shedding by tumor necrosis factor-alpha-converting enzyme (ADAM17). diagnostic usage,ongoing research,unassigned 3,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19457070&form=6&db=m Cellular prion protein coupling to TACE-dependent TNF-alpha shedding controls neurotransmitter catabolism in neuronal cells. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19485419&form=6&db=m High-resolution crystal structure of the snake venom metalloproteinase BaP1 complexed with a peptidomimetic: insight into inhibitor binding. therapeutic application,unassigned 4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19515085&form=6&db=m Tumorigenicity of cortical astrocyte cell line induced by the protease ADAM17. causal interaction,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19543557&form=6&db=m Exogenous nitric oxide inhibits shedding of ADAM17 substrates. causal interaction,unassigned 4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19581512&form=6&db=m Tumor necrosis factor-alpha-converting enzyme is a key regulator of agonist-induced cardiac hypertrophy and fibrosis. causal interaction,diagnostic usage,therapeutic application,unassigned 3,4,2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19601834&form=6&db=m ADAM17 as a therapeutic target in multiple diseases. causal interaction,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19603023&form=6&db=m Increased expression of ALCAM/CD166 in pancreatic cancer is an independent prognostic marker for poor survival and early tumour relapse. causal interaction,diagnostic usage,ongoing research,therapeutic application 1,2,3,1 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19620400&form=6&db=m Activation of endothelial intrinsic NF-{kappa}B pathway impairs protein C anticoagulation mechanism and promotes coagulation in endotoxemic mice. ongoing research,unassigned 2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19640509&form=6&db=m SLITRK1 Binds 14-3-3 and Regulates Neurite Outgrowth in a Phosphorylation-Dependent Manner. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19717015&form=6&db=m Preconditioning with sublethal ischemia or intermittent normobaric hyperoxia up-regulates glutamate transporters and tumor necrosis factor-alpha converting enzyme in the rat brain. causal interaction,ongoing research,unassigned 3,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19759332&form=6&db=m Selective and Specific Regulation of Ectodomain Shedding of Angiotensin-converting Enzyme 2 by Tumor Necrosis Factor {alpha}-converting Enzyme. causal interaction,therapeutic application,unassigned 3,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19772640&form=6&db=m Transcription factor Sp1 induces ADAM17 and contributes to tumor cell invasiveness under hypoxia. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,3,4,1 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19796498&form=6&db=m Cell-cell interaction promotes rat marrow stromal cell differentiation into endothelial cell via activation of TACE/TNF-alpha signaling. causal interaction,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19819120&form=6&db=m ADAM17_i33708A>G polymorphism interacts with dietary n-6 polyunsaturated fatty acids to modulate obesity risk in the Genetics of Lipid Lowering Drugs and Diet Network study. causal interaction,diagnostic usage,ongoing research,unassigned 4,2,2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19843672&form=6&db=m Sheddase Activity of Tumor Necrosis Factor-{alpha} Converting Enzyme Is Increased and Prognostically Valuable in Head and Neck Cancer. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,2,1 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19854762&form=6&db=m Induction of TNF-alpha-converting enzyme-ectodomain shedding by pathogenic autoantibodies. ongoing research,unassigned 2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19877183&form=6&db=m Increased tumor necrosis factor alpha-converting enzyme activity induces insulin resistance and hepatosteatosis in mice. causal interaction,therapeutic application,unassigned 4,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19951006&form=6&db=m Molecular modeling and biological effects of peptidomimetic inhibitors of TACE activity. ongoing research,therapeutic application,unassigned 1,2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19965619&form=6&db=m p38 mitogen-activated protein kinase activation during platelet storage: consequences for platelet recovery and hemostatic function in vivo. causal interaction,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20042582&form=6&db=m Essential roles of IL-6 trans-signaling in colonic epithelial cells, induced by the IL-6/soluble-IL-6 receptor derived from lamina propria macrophages, on the development of colitis-associated premalignant cancer in a murine model. causal interaction,diagnostic usage,ongoing research,unassigned 3,2,2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20064929&form=6&db=m P2Y2 nucleotide receptors mediate metalloprotease-dependent phosphorylation of epidermal growth factor receptor and ErbB3 in human salivary gland cells. causal interaction,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20070837&form=6&db=m Tumor necrosis factor-alpha-converting enzyme as a potential mediator of the influence of smoking on the response to treatment with narrowband ultraviolet B in psoriasis patients. causal interaction,therapeutic application,unassigned 1,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20098684&form=6&db=m MicroRNA-145 targets YES and STAT1 in colon cancer cells. causal interaction,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20110534&form=6&db=m Pathological neovascularization is reduced by inactivation of ADAM17 in endothelial cells but not in pericytes. diagnostic usage,ongoing research,unassigned 3,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20179991&form=6&db=m Development of predictive pharmacophore model for in silico screening, and 3D QSAR CoMFA and CoMSIA studies for lead optimization, for designing of potent tumor necrosis factor alpha converting enzyme inhibitors. therapeutic application,unassigned 4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20180536&form=6&db=m Potent arylsulfonamide inhibitors of tumor necrosis factor-alpha converting enzyme able to reduce activated leukocyte cell adhesion molecule shedding in cancer cell models. therapeutic application,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20184396&form=6&db=m ADAM-17: the enzyme that does it all. causal interaction,therapeutic application,unassigned 4,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20192217&form=6&db=m Anti-inflammatory bioactivities of honokiol through inhibition of protein kinase C, mitogen-activated protein kinase, and the NF-kappaB pathway to reduce LPS-induced TNFalpha and NO expression. ongoing research,unassigned 4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20197648&form=6&db=m Improved Synthesis of ADAM10 Inhibitor GI254023X. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20215529&form=6&db=m Metalloproteinase-dependent cleavage of neuregulin and autocrine stimulation of vascular endothelial cells. therapeutic application,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20300969&form=6&db=m ADAM-17 over-expression in gallbladder carcinoma correlates with poor prognosis of patients. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,4,4,3 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20303413&form=6&db=m Tumor necrosis factor-alpha converting enzyme: Implications for ocular inflammatory diseases. causal interaction,therapeutic application,unassigned 1,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20349256&form=6&db=m Anthranilate derivatives as TACE inhibitors: Docking based CoMFA and CoMSIA analyses. causal interaction,therapeutic application,unassigned 3,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20457810&form=6&db=m Pref-1 interacts with fibronectin to inhibit adipocyte differentiation. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20486929&form=6&db=m Tumor necrosis factor alpha converting enzyme: an encouraging target for various inflammatory disorders. causal interaction,therapeutic application,unassigned 4,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20529858&form=6&db=m Stimulation of platelet-derived growth factor receptor beta (PDGFRbeta) activates ADAM17 and promotes metalloproteinase-dependent cross-talk between the PDGFRbeta and epidermal growth factor receptor (EGFR) signaling pathways. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20570921&form=6&db=m Chemotherapy-induced activation of ADAM-17: a novel mechanism of drug resistance in colorectal cancer. causal interaction,therapeutic application,unassigned 4,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20603312&form=6&db=m Critical role of the disintegrin metalloprotease ADAM17 for intestinal inflammation and regeneration in mice. causal interaction,diagnostic usage,ongoing research,unassigned 4,1,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20826789&form=6&db=m Plasma kallikrein promotes epidermal growth factor receptor transactivation and signaling in vascular smooth muscle through direct activation of protease-activated receptors. causal interaction,therapeutic application,unassigned 4,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20871631&form=6&db=m A transforming Src mutant increases the bioavailability of EGFR ligands via stimulation of the cell-surface metalloproteinase ADAM17. causal interaction,ongoing research,therapeutic application,unassigned 3,3,2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21141511&form=6&db=m [Construction and identification of bait recombinant vector of tumor necrosis factor-alpha converting enzyme in the yeast two hybrid system]. ongoing research,therapeutic application,unassigned 2,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21148749&form=6&db=m Oncogenic Kras promotes chemotherapy-induced growth factor shedding via ADAM17. causal interaction,therapeutic application,unassigned 4,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21175594&form=6&db=m ADAM metallopeptidase domain 17 (ADAM17) is naturally processed through major histocompatibility complex (MHC) class I molecules and is a potential immunotherapeutic target in breast, ovarian and prostate cancers. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,4,4 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21194787&form=6&db=m The "A Disintegrin And Metalloproteases" ADAM10 and ADAM17: Novel drug targets with therapeutic potential? causal interaction,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21205091&form=6&db=m Activation of epidermal growth factor receptor signaling by the prostaglandin E(2) receptor EP4 pathway during gastric tumorigenesis. causal interaction,diagnostic usage,therapeutic application,unassigned 2,1,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21240579&form=6&db=m ADAM12 and ADAM17 Gene Expression in Laser-capture Microdissected and Non-microdissected Breast Tumors. causal interaction,diagnostic usage,ongoing research,unassigned 4,1,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21314837&form=6&db=m What Blood Temperature for an Ex Vivo Extracorporeal Circuit? diagnostic usage,ongoing research,unassigned 1,2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21435459&form=6&db=m Genotypic and phenotypic characterization of side population of gastric cancer cell lines. causal interaction,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21480393&form=6&db=m ADAM17 promotes glioma cell malignant phenotype. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,4,1 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21501859&form=6&db=m Increased expression of ADAM12 and ADAM17 genes in laser-capture microdissected breast cancers and correlations with clinical and pathological characteristics. causal interaction,diagnostic usage,ongoing research,unassigned 4,3,3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21563828&form=6&db=m Angiotensin-converting enzyme 2 ectodomain shedding cleavage-site identification: determinants and constraints. causal interaction,diagnostic usage,unassigned 4,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21645559&form=6&db=m TACE cleaves neogenin to desensitize cortical neurons to the repulsive guidance molecule. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21752713&form=6&db=m ADAM17: a molecular switch to control inflammation and tissue regeneration. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21837402&form=6&db=m ADAM17 regulates prostate cancer cell proliferation through mediating cell cycle progression by EGFR/PI3K/AKT pathway. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,4,1 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21906355&form=6&db=m The ADAMs family of proteases: new biomarkers and therapeutic targets for cancer? causal interaction,diagnostic usage,unassigned 2,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22010916&form=6&db=m Inflammatory skin and bowel disease linked to ADAM17 deletion. causal interaction,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22105359&form=6&db=m The unfolded protein response controls induction and activation of ADAM17/TACE by severe hypoxia and ER stress. causal interaction,therapeutic application,unassigned 3,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22139867&form=6&db=m Prognostic value of ADAM17 in human gastric cancer. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,4,3 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22200661&form=6&db=m ADAM17 targets MMP-2 and MMP-9 via EGFR-MEK-ERK pathway activation to promote prostate cancer cell invasion. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,4,3 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22319556&form=6&db=m Investigation of the role of TNF-? converting enzyme (TACE) in the inhibition of cell surface and soluble TNF-? production by acute ethanol exposure. therapeutic application,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22385614&form=6&db=m Free Energy Calculations on Snake Venom Metalloproteinase BaP1. therapeutic application,unassigned 4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22509934&form=6&db=m A novel bispecific single-chain antibody for ADAM17 and CD3 induces T-cell-mediated lysis of prostate cancer cells. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,3,4,1 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22550340&form=6&db=m TACE activation by MAPK-mediated regulation of cell surface dimerization and TIMP3 association. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22668812&form=6&db=m Upregulated Expression of ADAM17 Is a Prognostic Marker for Patients With Gastric Cancer. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,4,1 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22696231&form=6&db=m Brief Report: Requirement of TACE/ADAM17 for Hair Follicle Bulge Niche Establishment. causal interaction,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22713436&form=6&db=m Does Adam17 cause the destruction of anchoring fibers via shedding tumor necrosis factor ? in bullous pemphigoid and dermatitis herpetiformis? unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22772468&form=6&db=m Differentiation-induced skin cancer suppression by FOS, p53, and TACE/ADAM17. therapeutic application,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22792380&form=6&db=m Anti-tumour effects of a specific anti-ADAM17 antibody in an ovarian cancer model in vivo. ongoing research,therapeutic application,unassigned 2,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22833676&form=6&db=m A disintegrin and metalloproteinase 17 (ADAM17) and epidermal growth factor receptor (EGFR) signaling drive the epithelial response to Staphylococcus aureus toxic shock syndrome toxin-1 (TSST-1). causal interaction,ongoing research,unassigned 3,2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22940887&form=6&db=m ADAM17-overexpressing breast cancer cells selectively targeted by antibody-toxin conjugates. causal interaction,therapeutic application,unassigned 1,3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22967992&form=6&db=m ADAM-17: a novel therapeutic target for triple negative breast cancer. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,2,4,4 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23173124&form=6&db=m The role of microRNA in metastatic colorectal cancer and its significance in cancer prognosis and treatment. causal interaction,diagnostic usage,therapeutic application,unassigned 3,3,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23231541&form=6&db=m Novel methods and strategies in the discovery of TACE inhibitors. causal interaction,therapeutic application,unassigned 1,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23251384&form=6&db=m ADAM17 silencing in mouse colon carcinoma cells: the effect on tumoricidal cytokines and angiogenesis. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,4,3 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23415892&form=6&db=m ADAM17, shedding, TACE as therapeutic targets. causal interaction,therapeutic application,unassigned 4,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23441135&form=6&db=m MicroRNA-145 Targets the Metalloprotease ADAM17 and Is Suppressed in Renal Cell Carcinoma Patients. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,1,2,1 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23475633&form=6&db=m ADAM17 is overexpressed in non-small cell lung cancer and its expression correlates with poor patient survival. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,4,3 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23521534&form=6&db=m The membrane-proximal domain of ADAM17 represents the putative molecular switch of its shedding activity operated by protein-disulfide isomerase. therapeutic application,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23526433&form=6&db=m Shedding of endogenous MHC class I-related chain molecules A and B (MICA and MICB) from different human tumor entities: Heterogeneous involvement of the a disintegrin and metalloproteases 10 and 17 (ADAM10 and ADAM17). ongoing research,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23545805&form=6&db=m The disintegrin domain of ADAM17 antagonises fibroblast?carcinoma cell interactions. diagnostic usage,ongoing research,unassigned 2,3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23625205&form=6&db=m ADAM17 mediates hypoxia-induced drug resistance in hepatocellular carcinoma cells through activation of EGFR/PI3K/Akt pathway. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,1,4,3 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23639813&form=6&db=m A disintegrin and metalloproteinase 17 regulates TNF and TNFR1 levels in inflammation and liver regeneration in mice. causal interaction,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23641036&form=6&db=m Bone morphogenetic protein 15 and fibroblast growth factor 10 enhance cumulus expansion, glucose uptake, and expression of genes in the ovulatory cascade during in vitro maturation of bovine cumulus-oocyte complexes. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23645517&form=6&db=m Molecular Profiling of ADAM12 and ADAM17 Genes in Human Malignant Melanoma. causal interaction,diagnostic usage,ongoing research,unassigned 4,4,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23684931&form=6&db=m Human breast cancer-associated fibroblasts enhance cancer cell proliferation through increased TGF-? cleavage by ADAM17. causal interaction,ongoing research,therapeutic application,unassigned 4,4,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23729230&form=6&db=m TACE-dependent TGF? shedding drives triple-negative breast cancer cell invasion. causal interaction,diagnostic usage,unassigned 3,3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23732913&form=6&db=m ADAM17 controls endochondral ossification by regulating terminal differentiation of chondrocytes. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23969955&form=6&db=m Mammalian iRhoms have distinct physiological functions including an essential role in TACE regulation. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24072428&form=6&db=m Tumor necrosis factor-alpha-converting enzyme activities and tumor-associated macrophages in breast cancer. causal interaction,ongoing research,unassigned 2,2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24130797&form=6&db=m Differential surface expression of ADAM10 and ADAM17 on human T lymphocytes and tumor cells. diagnostic usage,ongoing research,unassigned 3,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24197832&form=6&db=m Breast tumor cell TACE-shed MCSF promotes pro-angiogenic macrophages through NF-?B signaling. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24319187&form=6&db=m Therapeutic applications: natural killer cells in the clinic. ongoing research,therapeutic application,unassigned 3,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24336074&form=6&db=m ADAM17 is a survival factor for microglial cells in vitro and in vivo after spinal cord injury in mice. causal interaction,ongoing research,unassigned 1,3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24338472&form=6&db=m Polo-like kinase 2, a novel ADAM17 signaling component, regulates tumor necrosis factor ? ectodomain shedding. causal interaction,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24361716&form=6&db=m Glycosylation of a disintegrin and metalloprotease 17 affects its activity and inhibition. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24424050&form=6&db=m Protein kinase C (PKC) increases TACE/ADAM17 enzyme activity in porcine ovarian somatic cells, which is essential for granulosa cell luteinization and oocyte maturation. causal interaction,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24462774&form=6&db=m Dissociated presenilin-1 and TACE processing of ErbB4 in lung alveolar type II cell differentiation. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24625128&form=6&db=m Deciphering the Role of the ADAM17-Dependent Secretome in Cell Signaling. diagnostic usage,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24626788&form=6&db=m ADAM17 silencing suppresses the migration and invasion of non-small cell lung cancer. causal interaction,ongoing research,therapeutic application,unassigned 3,3,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24635658&form=6&db=m LC-MS Based Cleavage Site Profiling of the Proteases ADAM10 and ADAM17 Using Proteome-Derived Peptide Libraries. causal interaction,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24736554&form=6&db=m miR-221/222 control luminal breast cancer tumor progression by regulating different targets. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24738885&form=6&db=m Insights into desmosome biology from inherited human skin disease and cardiocutaneous syndromes. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24780186&form=6&db=m MicroRNA-152 targets ADAM17 to suppress NSCLC progression. therapeutic application,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24780758&form=6&db=m Metalloprotease-mediated tumor cell shedding of B7-H6, the ligand of the natural killer cell-activating receptor NKp30. ongoing research,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24793016&form=6&db=m ADAM17 is associated with EMMPRIN and predicts poor prognosis in patients with uterine cervical carcinoma. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,4,3 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24843386&form=6&db=m Gallic acid reduces cell viability, proliferation, invasion and angiogenesis in human cervical cancer cells. causal interaction,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24980871&form=6&db=m The P2/P2' sites affect the substrate cleavage of TNF-? converting enzyme (TACE). causal interaction,therapeutic application,unassigned 1,3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24996774&form=6&db=m A novel marker ADAM17 for clear cell renal cell carcinomas: Implication for patients' prognosis. diagnostic usage,ongoing research,therapeutic application,unassigned 2,3,3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25013379&form=6&db=m Targeting the sheddase activity of ADAM17 by an anti-ADAM17 antibody D1(A12) inhibits head and neck squamous cell carcinoma cell proliferation and motility via blockage of bradykinin induced HERs transactivation. causal interaction,ongoing research,therapeutic application,unassigned 4,4,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25077560&form=6&db=m Senescence-associated release of transmembrane proteins involves proteolytic processing by ADAM17 and microvesicle shedding. ongoing research,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25124714&form=6&db=m ADAM10 correlates with uveal melanoma metastasis and promotes in vitro invasion. causal interaction,therapeutic application,unassigned 3,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25171914&form=6&db=m ADAM17 at the interface between inflammation and autoimmunity. causal interaction,diagnostic usage,therapeutic application,unassigned 4,2,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25186737&form=6&db=m TACE/ADAM17 is essential for oligodendrocyte development and CNS myelination. causal interaction,unassigned 4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25251383&form=6&db=m Synthesis of [(3) H], [(13) C3 , (15) N], and [(14) C]SCH 900567: an inhibitor of TNF-? (tumor necrosis factor alpha) converting enzyme (TACE). causal interaction,therapeutic application,unassigned 3,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25351873&form=6&db=m A disintegrin and metalloproteinase 17 mRNA and protein expression in esophageal squamous cell carcinoma, as well as its clinicopathological factors and prognosis. causal interaction,diagnostic usage,ongoing research,unassigned 3,4,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25364437&form=6&db=m Diagnostic and prognostic value of a disintegrin and metalloproteinase-17 in patients with gliomas. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,4,4 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25367431&form=6&db=m EpCAM is decreased but is still present in uterine epithelial cells during early pregnancy in the rat: potential mechanism for maintenance of mucosal integrity during implantation. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25598752&form=6&db=m Reduction of Serum ADAM17 Level Accompanied with Decreased Cytokines after Abatacept Therapy in Patients with Rheumatoid Arthritis. causal interaction,diagnostic usage,therapeutic application,unassigned 4,4,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25610924&form=6&db=m A metal-based tumour necrosis factor-alpha converting enzyme inhibitor. therapeutic application,unassigned 4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25786367&form=6&db=m Prognostic significance of ADAM17 expression in patients with gastric cancer who underwent curative gastrectomy. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,4,2 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25817572&form=6&db=m Differential regulation of TROP2 release by PKC isoforms through vesicles and ADAM17. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25912030&form=6&db=m A transmembrane C-terminal fragment of syndecan-1 is generated by the metalloproteinase ADAM17 and promotes lung epithelial tumor cell migration and lung metastasis formation. causal interaction,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25926412&form=6&db=m The Antiatherogenic Effect of Fish Oil in Male Mice Is Associated with a Diminished Release of Endothelial ADAM17 and ADAM10 Substrates. causal interaction,unassigned 2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25948294&form=6&db=m A Monoclonal Antibody to ADAM17 Inhibits Tumor Growth by Inhibiting EGFR and Non-EGFR-Mediated Pathways. causal interaction,ongoing research,therapeutic application,unassigned 2,4,2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26108729&form=6&db=m The sorting protein PACS-2 promotes ErbB signalling by regulating recycling of the metalloproteinase ADAM17. causal interaction,ongoing research,therapeutic application,unassigned 4,2,3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26176220&form=6&db=m ADAM17 Promotes Motility, Invasion, and Sprouting of Lymphatic Endothelial Cells. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,1,3 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26190895&form=6&db=m Effect of Clarithromycin on the Expression of UL16-Binding Protein 2 in Human Cells. ongoing research,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26348730&form=6&db=m Extracellular Juxtamembrane Segment of ADAM17 Interacts with Membranes and Is Essential for Its Shedding Activity. causal interaction,unassigned 4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26535007&form=6&db=m Deletions in the cytoplasmic domain of iRhom1 and iRhom2 promote shedding of the TNF receptor by the protease ADAM17. causal interaction,ongoing research,unassigned 2,3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26655882&form=6&db=m Gene silencing of TACE enhances plaque stability and improves vascular remodeling in a rabbit model of atherosclerosis. ongoing research,therapeutic application,unassigned 1,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26723565&form=6&db=m Microparticles generated during chronic cerebral ischemia increase the permeability of microvascular endothelial barriers in vitro. therapeutic application,unassigned 4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26744411&form=6&db=m A Disintegrin and Metalloproteinase Domain 17 Regulates Colorectal Cancer Stem Cells and Chemosensitivity Via Notch1 Signaling. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,3,4,3 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27046120&form=6&db=m Interphotoreceptor Retinoid-Binding Protein Mitigates Cellular Oxidative Stress and Mitochondrial Dysfunction Induced by All-trans-Retinal. causal interaction,unassigned 2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27076628&form=6&db=m Secretome Signature Identifies ADAM17 as Novel Target for Radiosensitization of Non-Small Cell Lung Cancer. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,3,4,4 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27077118&form=6&db=m Epithelial Cell-Derived a Disintegrin and Metalloproteinase-17 Confers Resistance to Colonic Inflammation Through EGFR Activation. causal interaction,ongoing research,therapeutic application,unassigned 4,4,2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27110571&form=6&db=m Expression of Migration-Related Genes in Human Colorectal Cancer and Activity of a Disintegrin and Metalloproteinase 17. causal interaction,diagnostic usage,ongoing research,unassigned 1,4,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27115328&form=6&db=m The ADAMs family of proteases as targets for the treatment of cancer. causal interaction,therapeutic application,unassigned 4,3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27221510&form=6&db=m ADAM17-siRNA inhibits MCF-7 breast cancer through EGFR-PI3K-AKT activation. causal interaction,ongoing research,therapeutic application,unassigned 1,4,2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27256961&form=6&db=m Regulation of A disintegrin and metalloproteinase (ADAM) family sheddases ADAM10 and ADAM17: The emerging role of tetraspanins and rhomboids. causal interaction,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27467923&form=6&db=m ADAM10 new selective inhibitors reduce NKG2D ligand release sensitizing Hodgkin lymphoma cells to NKG2D-mediated killing. causal interaction,therapeutic application,unassigned 4,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27469341&form=6&db=m Targeting ADAM17 Sheddase Activity In Cancer. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,1,3,4 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27489286&form=6&db=m ADAM17 is a tumor promoter and therapeutic target in Western diet-associated colon cancer. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,3,4,4 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27541285&form=6&db=m Metalloproteinases ADAM10 and ADAM17 Mediate Migration and Differentiation in Glioblastoma Sphere-Forming Cells. causal interaction,ongoing research,therapeutic application,unassigned 3,3,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27573075&form=6&db=m A-Disintegrin and Metalloproteinase (ADAM) 17 Enzymatically Degrades Interferon-gamma. causal interaction,ongoing research,therapeutic application,unassigned 3,3,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27576135&form=6&db=m Mass spectrometry-based proteomics revealed Glypican-1 as a novel ADAM17 substrate. causal interaction,ongoing research,therapeutic application,unassigned 4,1,2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27599715&form=6&db=m Stimulated release and functional activity of surface expressed metalloproteinase ADAM17 in exosomes. causal interaction,ongoing research,unassigned 1,3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27692848&form=6&db=m Changes in expressions of ADAM9, 10, and 17 as well as ?-secretase activity in renal cell carcinoma. causal interaction,diagnostic usage,therapeutic application,unassigned 3,4,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27738494&form=6&db=m ADAM17 in tumor associated leukocytes regulates inflammatory mediators and promotes mammary tumor formation. causal interaction,therapeutic application,unassigned 4,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27779657&form=6&db=m ADAM17 promotes epithelial-mesenchymal transition via TGF-?/Smad pathway in gastric carcinoma cells. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,1,2,4 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27878499&form=6&db=m Therapeutic potential of ADAM17 modulation in gastric cancer through regulation of the EGFR and TNF-? signalling pathways. causal interaction,diagnostic usage,ongoing research,unassigned 4,3,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27895032&form=6&db=m Molecular Pathways: Receptor Ectodomain Shedding in Treatment, Resistance, and Monitoring of Cancer. causal interaction,diagnostic usage,unassigned 3,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27941799&form=6&db=m Inhibition of Notch pathway arrests PTEN-deficient advanced prostate cancer by triggering p27-driven cellular senescence. causal interaction,therapeutic application,unassigned 4,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27982031&form=6&db=m Harnessing the natural inhibitory domain to control TNF? Converting Enzyme (TACE) activity in vivo. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28056193&form=6&db=m Reduced CD62L Expression on T Cells and Increased Soluble CD62L Levels Predict Molecular Response to Tyrosine Kinase Inhibitor Therapy in Early Chronic-Phase Chronic Myelogenous Leukemia. causal interaction,diagnostic usage,therapeutic application,unassigned 2,1,2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28084316&form=6&db=m TNF? drives pulmonary arterial hypertension by suppressing the BMP type-II receptor and altering NOTCH signalling. ongoing research,therapeutic application,unassigned 3,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28104813&form=6&db=m Structural modeling defines transmembrane residues in ADAM17 that are crucial for Rhbdf2-ADAM17-dependent proteolysis. causal interaction,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28109308&form=6&db=m Semaphorin 7A as a potential immune regulator and promising therapeutic target in rheumatoid arthritis. ongoing research,unassigned 2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28160627&form=6&db=m Interleukin-11-driven gastric tumourigenesis is independent of trans-signalling. causal interaction,diagnostic usage,unassigned 2,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28350885&form=6&db=m Glutamate-dependent ectodomain shedding of neuregulin-1 type II precursors in rat forebrain neurons. causal interaction,ongoing research,therapeutic application,unassigned 1,1,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28414309&form=6&db=m Tumor-derived fibulin-3 activates pro-invasive NF-?B signaling in glioblastoma cells and their microenvironment. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28512108&form=6&db=m Clinical Relevance and Role of Neuronal AT1 Receptors in ADAM17-Mediated ACE2 Shedding in Neurogenic Hypertension. causal interaction,diagnostic usage,ongoing research,unassigned 3,4,3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28637950&form=6&db=m ADAM17 regulates TNF-? expression upon lipopolysaccharide stimulation in oral keratinocytes. causal interaction,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28666872&form=6&db=m Disruption of TACE-filamin interaction can inhibit TACE-mediated ectodomain shedding. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28705384&form=6&db=m The shedding protease ADAM17: Physiology and pathophysiology. causal interaction,therapeutic application,unassigned 1,3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29029414&form=6&db=m Targeting ADAM17 inhibits human colorectal adenocarcinoma progression and tumor-initiating cell frequency. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,1,3,1 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29056164&form=6&db=m ADAM17, a New Player in the Pathogenesis of Chronic Kidney Disease-Mineral and Bone Disorder. causal interaction,diagnostic usage,ongoing research,unassigned 4,2,2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29131255&form=6&db=m The correlation between the expression of ADAM17, EGFR and Ki-67 in malignant gliomas. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,2,2 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29150960&form=6&db=m Epithelial cell adhesion molecule fragments and signaling in primary human liver cells. ongoing research,therapeutic application,unassigned 3,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29171106&form=6&db=m Autophagy regulates cisplatin-induced stemness and chemoresistance via the upregulation of CD44, ABCB1 and ADAM17 in oral squamous cell carcinoma. causal interaction,diagnostic usage,unassigned 3,2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29180185&form=6&db=m ADAM-17 expression is enhanced by FoxM1 and is a poor prognostic sign in gastric carcinoma. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,3,3 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29187866&form=6&db=m Modification of proteolytic activity matrix analysis (PrAMA) to measure ADAM10 and ADAM17 sheddase activities in cell and tissue lysates. diagnostic usage,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29230082&form=6&db=m Recent Advances in ADAM17 Research: A Promising Target for Cancer and Inflammation. causal interaction,therapeutic application,unassigned 3,2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29308299&form=6&db=m Platelet-mediated shedding of NKG2D ligands impairs NK cell immune-surveillance of tumor cells. causal interaction,diagnostic usage,unassigned 1,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29393483&form=6&db=m Short hairpin RNA-mediated gene silencing of ADAM17 inhibits the growth of breast cancer MCF?7 cells in vitro and in vivo and its mechanism of action. causal interaction,ongoing research,unassigned 4,3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29411180&form=6&db=m ADAM-17 is expressed in the inflammatory myopathy and is involved with interstitial lung disease. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,4,4 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29472497&form=6&db=m ADAM17 is required for EGF-R-induced intestinal tumors via IL-6 trans-signaling. causal interaction,ongoing research,therapeutic application,unassigned 4,3,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29499360&form=6&db=m Ursolic acid prevents angiotensin II-induced abdominal aortic aneurysm in apolipoprotein E-knockout mice. causal interaction,ongoing research,unassigned 3,2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29662625&form=6&db=m ADAM17 inhibition enhances platinum efficiency in ovarian cancer. causal interaction,diagnostic usage,ongoing research,therapeutic application 2,1,2,4 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29776401&form=6&db=m ADAM-17 is a poor prognostic indicator for patients with hilar cholangiocarcinoma and is regulated by FoxM1. causal interaction,diagnostic usage,ongoing research,unassigned 3,4,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29923217&form=6&db=m Expression of the ectodomain-releasing protease ADAM17 is directly regulated by the osteosarcoma and bone-related transcription factor RUNX2. causal interaction,diagnostic usage,unassigned 4,3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29966664&form=6&db=m ADAM17 promotes cell migration and invasion through the integrin ?1 pathway in hepatocellular carcinoma. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,4,4 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29978334&form=6&db=m Anti-ADAM17 monoclonal antibody MEDI3622 increases IFN? production by human NK cells in the presence of antibody-bound tumor cells. ongoing research,unassigned 4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30009514&form=6&db=m Current strategies exploiting NK-cell therapy to treat haematologic malignancies. causal interaction,therapeutic application,unassigned 1,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30026855&form=6&db=m ADAM10 Sheddase Activity is a Potential Lung-Cancer Biomarker. causal interaction,diagnostic usage,ongoing research,unassigned 4,3,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30055896&form=6&db=m The Rhomboid Superfamily: Structural Mechanisms and Chemical Biology Opportunities. causal interaction,unassigned 4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30065191&form=6&db=m Bisphenol-A and Nonylphenol Induce Apoptosis in Reproductive Tract Cancer Cell Lines by the Activation of ADAM17. ongoing research,therapeutic application,unassigned 3,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30102846&form=6&db=m Synthesis and in vitro Evaluation of ADAM10 and ADAM17 Highly Selective Bioimaging Probes. causal interaction,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30297396&form=6&db=m iNOS promotes CD24+CD133+ liver cancer stem cell phenotype through a TACE/ADAM17-dependent Notch signaling pathway. causal interaction,diagnostic usage,therapeutic application,unassigned 4,3,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30395261&form=6&db=m Enhanced expression of TACE contributes to elevated levels of sVCAM-1 in endometriosis. causal interaction,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30551445&form=6&db=m Nox1/4 dual inhibitor GKT137831 attenuates hypertensive cardiac remodelling associating with the inhibition of ADAM17-dependent proinflammatory cytokines-induced signalling pathways in the rats with abdominal artery constriction. ongoing research,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30616034&form=6&db=m Decoding the enigma of antiviral crisis: Does one target molecule regulate all? causal interaction,ongoing research,therapeutic application,unassigned 3,2,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30675599&form=6&db=m Rapid and sensitive detection of the activity of ADAM17 using a graphene oxide-based fluorescence sensor. causal interaction,therapeutic application,unassigned 4,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30709842&form=6&db=m The role of NF-?B and Elk-1 in the regulation of mouse ADAM17 expression. causal interaction,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30729673&form=6&db=m L-Selectin Expression Is Influenced by Phosphatase Activity in Chronic Lymphocytic Leukemia. causal interaction,ongoing research,unassigned 1,2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30786043&form=6&db=m Role of ADAM17 as a regulatory checkpoint of CD16A in NK cells and as a potential target for cancer immunotherapy. causal interaction,ongoing research,therapeutic application,unassigned 3,3,2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30833304&form=6&db=m ADAM17 selectively activates the IL-6 trans-signaling/ERK MAPK axis in KRAS-addicted lung cancer. ongoing research,therapeutic application,unassigned 1,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30851105&form=6&db=m EGFR-Dependent IL8 Production by Airway Epithelial Cells After Exposure to the Food Flavoring Chemical 2,3-Butanedione. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30941646&form=6&db=m Genetic Association Between NGFR, ADAM17 Gene Polymorphism, and Parkinson's Disease in the Chinese Han Population. causal interaction,ongoing research,unassigned 1,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30992230&form=6&db=m The metalloprotease ADAM17 in inflammation and cancer. causal interaction,therapeutic application,unassigned 4,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31060243&form=6&db=m Functional Characterization of Colon Cancer-Associated Mutations in ADAM17: Modifications in the Pro-Domain Interfere with Trafficking and Maturation. causal interaction,ongoing research,unassigned 2,3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31141400&form=6&db=m Role of ADAM17 in kidney disease. causal interaction,ongoing research,therapeutic application,unassigned 4,3,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31257400&form=6&db=m The ADAM17 Protease Promotes Tobacco Smoke Carcinogen-induced Lung Tumourigenesis. causal interaction,ongoing research,therapeutic application,unassigned 3,3,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31295519&form=6&db=m Store-operated calcium entry (SOCE) contributes to phosphorylation of p38 MAPK and suppression of TNF-? signalling in the intestinal epithelial cells. ongoing research,therapeutic application,unassigned 1,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31438559&form=6&db=m ADAM17: An Emerging Therapeutic Target for Lung Cancer. causal interaction,therapeutic application,unassigned 3,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31593799&form=6&db=m ADAM proteases: Emerging role and targeting of the non-catalytic domains. causal interaction,therapeutic application,unassigned 1,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31619190&form=6&db=m Ionizing radiation increases the endothelial permeability and the transendothelial migration of tumor cells through ADAM10-activation and subsequent degradation of VE-cadherin. ongoing research,unassigned 4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31662485&form=6&db=m iRhom2 and TNF: Partners or enemies? unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31662486&form=6&db=m iRhom2 inhibits bile duct obstruction-induced liver fibrosis. ongoing research,unassigned 4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31694340&form=6&db=m ADAM17 Activity and IL-6 Trans-Signaling in Inflammation and Cancer. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,4,4 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31704085&form=6&db=m A Genetically Engineered Primary Human Natural Killer Cell Platform for Cancer Immunotherapy. causal interaction,therapeutic application,unassigned 1,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31749431&form=6&db=m In Silico Screening for Anti-Inflammatory Bioactive Molecules from Ayurvedic Decoction, Balaguluchyadi Kashayam. diagnostic usage,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31771880&form=6&db=m B cell ADAM17 controls T cell independent humoral immune responses through regulation of TACI and CD138. causal interaction,unassigned 4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32060096&form=6&db=m ADAM17 stabilizes its interacting partner inactive Rhomboid 2 (iRhom2) but not inactive Rhomboid 1 (iRhom1). unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32222277&form=6&db=m Distance dependent shedding of IL-6R. causal interaction,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32245188&form=6&db=m A Disintegrin and Metalloproteinase 9 (ADAM9) in Advanced Hepatocellular Carcinoma and Their Role as a Biomarker During Hepatocellular Carcinoma Immunotherapy. causal interaction,diagnostic usage,ongoing research,unassigned 4,3,2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32319567&form=6&db=m Lewis antigen?negative pancreatic cancer: An aggressive subgroup. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32363112&form=6&db=m ADAM10 and ADAM17 cleave PD-L1 to mediate PD-(L)1 inhibitor resistance. causal interaction,diagnostic usage,therapeutic application,unassigned 4,2,3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32400009&form=6&db=m Mechanisms of site-specific dephosphorylation and kinase opposition imposed by PP2A regulatory subunits. causal interaction,ongoing research,therapeutic application,unassigned 3,3,2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32450419&form=6&db=m HPP1 Ectodomain Shedding is Mediated by ADAM17 and is Necessary for Tumor Suppression in Colon Cancer. causal interaction,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32610677&form=6&db=m Prognostic Significance of ADAM17 for Gastric Cancer Survival: A Meta-Analysis. causal interaction,diagnostic usage,therapeutic application,unassigned 4,4,3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32619562&form=6&db=m TNF?-Erk1/2 signaling pathway-regulated SerpinE1 and SerpinB2 are involved in lipopolysaccharide-induced porcine granulosa cell proliferation. causal interaction,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32679831&form=6&db=m Caveolae-Associated Protein 3 (Cavin-3) Influences Adipogenesis via TACE-Mediated Pref-1 Shedding. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32822911&form=6&db=m A combinational approach to restore cytokine balance and to inhibit virus growth may promote patient recovery in severe COVID-19 cases. causal interaction,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32889897&form=6&db=m MiR-338-3p inhibits cell migration and invasion in human hypopharyngeal cancer via downregulation of ADAM17. causal interaction,ongoing research,therapeutic application,unassigned 4,3,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33042435&form=6&db=m Tetraspanin CD9 interacts with ?-secretase to enhance its oncogenic function in pancreatic cancer. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33100908&form=6&db=m ADAM17 promotes the invasion of hepatocellular carcinoma via upregulation MMP21. causal interaction,diagnostic usage,ongoing research,unassigned 4,3,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33143292&form=6&db=m Functional Characterization of Colon-Cancer-Associated Variants in ADAM17 Affecting the Catalytic Domain. causal interaction,ongoing research,unassigned 3,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33239231&form=6&db=m Hypothesis: Alpha-1-antitrypsin is a promising treatment option for COVID-19. causal interaction,ongoing research,therapeutic application,unassigned 3,1,2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33531686&form=6&db=m More light on cancer and COVID-19 reciprocal interaction. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33552057&form=6&db=m Evaluation of Proteoforms of the Transmembrane Chemokines CXCL16 and CX3CL1, Their Receptors, and Their Processing Metalloproteinases ADAM10 and ADAM17 in Proliferative Diabetic Retinopathy. ongoing research,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33571627&form=6&db=m A wake-like state in vitro induced by transmembrane TNF/soluble TNF receptor reverse signaling. therapeutic application,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33575814&form=6&db=m Contribution of ADAM17 and related ADAMs in cardiovascular diseases. causal interaction,diagnostic usage,unassigned 1,3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33579029&form=6&db=m Strategies to Target ADAM17 in Disease: From its Discovery to the iRhom Revolution. diagnostic usage,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33672843&form=6&db=m Expression of ADAM Proteases in Bladder Cancer Patients with BCG Failure: A Pilot Study. causal interaction,diagnostic usage,ongoing research,unassigned 3,4,3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33904577&form=6&db=m Implications of ADAM17 activation for hyperglycaemia, obesity and type 2 diabetes. causal interaction,ongoing research,therapeutic application,unassigned 3,2,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33922533&form=6&db=m ADAM17 Inhibition Increases the Impact of Cisplatin Treatment in Ovarian Cancer Spheroids. causal interaction,ongoing research,therapeutic application,unassigned 4,4,4,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33953303&form=6&db=m Functionally confirmed compound heterozygous ADAM17 missense loss-of-function variants cause neonatal inflammatory skin and bowel disease 1. therapeutic application,unassigned 1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33957124&form=6&db=m Targeted truncation of the ADAM17 cytoplasmic domain in mice results in protein destabilization and a hypomorphic phenotype. causal interaction,therapeutic application,unassigned 3,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34182543&form=6&db=m Molecular switch in human diseases-disintegrin and metalloproteinases, ADAM17. unassigned - 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34192832&form=6&db=m The role of ADAM17 during liver damage. causal interaction,unassigned 2,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34208863&form=6&db=m Regulation of Platelet-Derived ADAM17: A Biomarker Approach for Breast Cancer? causal interaction,therapeutic application,unassigned 4,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34224305&form=6&db=m Rosmarinic acid inhibits proliferation and migration, promotes apoptosis and enhances cisplatin sensitivity of melanoma cells through inhibiting ADAM17/EGFR/AKT/GSK3? axis. ongoing research,therapeutic application,unassigned 4,1,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34362154&form=6&db=m ADAM 17 and Epithelial-to-Mesenchymal Transition: The Evolving Story and Its Link to Fibrosis and Cancer. causal interaction,unassigned 3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34367174&form=6&db=m Activation of ADAM17 by IL-15 Limits Human NK Cell Proliferation. causal interaction,therapeutic application,unassigned 1,3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34367416&form=6&db=m ADAM17 and NF-?B p65 form a positive feedback loop that facilitates human esophageal squamous cell carcinoma cell viability. causal interaction,ongoing research,unassigned 2,3,0 3.4.24.86 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34402747&form=6&db=m In-silico evidence of ADAM metalloproteinase pathology in cancer signaling networks. causal interaction,diagnostic usage,therapeutic application,unassigned 3,1,4,0 3.4.24.86 Nephrosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27706571&form=6&db=m Effects of Shenkangling intervention on the MAPK pathway in rats with doxorubicin-induced nephropathy. unassigned - 3.4.24.86 Nervous System Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26426268&form=6&db=m Neuronal ADAM10 Promotes Outgrowth of Small-Caliber Myelinated Axons in the Peripheral Nervous System. causal interaction,therapeutic application,unassigned 3,2,0 3.4.24.86 Neuralgia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30586315&form=6&db=m Impaired mechanical, heat, and cold nociception in a murine model of genetic TACE/ADAM17 knockdown. causal interaction,therapeutic application,unassigned 4,2,0 3.4.24.86 Neuroblastoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20506406&form=6&db=m Taiwan cobra phospholipase A2 elicits posttranscriptional up-regulation of ADAM17 in human neuroblastoma SK-N-SH cells. ongoing research,therapeutic application,unassigned 2,1,0 3.4.24.86 Neuroblastoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23257508&form=6&db=m Carnosic acid suppresses the production of amyloid-? 1-42 by inducing the metalloprotease gene TACE/ADAM17 in SH-SY5Y human neuroblastoma cells. causal interaction,ongoing research,therapeutic application,unassigned 3,3,2,0 3.4.24.86 Neuroblastoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33556560&form=6&db=m Phenanthroline impairs ?APP processing and expression, increases p53 protein levels and induces cell cycle arrest in human neuroblastoma cells. causal interaction,ongoing research,therapeutic application,unassigned 3,4,3,0 3.4.24.86 Neurodegenerative Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21194787&form=6&db=m The "A Disintegrin And Metalloproteases" ADAM10 and ADAM17: Novel drug targets with therapeutic potential? causal interaction,unassigned 3,0 3.4.24.86 Neurodegenerative Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24635658&form=6&db=m LC-MS Based Cleavage Site Profiling of the Proteases ADAM10 and ADAM17 Using Proteome-Derived Peptide Libraries. causal interaction,unassigned 3,0 3.4.24.86 Neurodegenerative Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33375653&form=6&db=m Activation of Kinin B1R Upregulates ADAM17 and Results in ACE2 Shedding in Neurons. unassigned - 3.4.24.86 Neuroinflammatory Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18621108&form=6&db=m Diverse roles of matrix metalloproteinases and tissue inhibitors of metalloproteinases in neuroinflammation and cerebral ischemia. causal interaction,unassigned 3,0 3.4.24.86 Neuroinflammatory Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31236626&form=6&db=m Functions of 'A disintegrin and metalloproteases (ADAMs)' in the mammalian nervous system. causal interaction,unassigned 3,0 3.4.24.86 Neuroinflammatory Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33374371&form=6&db=m The Gut-Brain Axis in Autism Spectrum Disorder: A Focus on the Metalloproteases ADAM10 and ADAM17. causal interaction,unassigned 3,0 3.4.24.86 Non-alcoholic Fatty Liver Disease http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28751722&form=6&db=m Hepatocyte specific TIMP3 expression prevents diet dependent fatty liver disease and hepatocellular carcinoma. causal interaction,therapeutic application,unassigned 4,1,0 3.4.24.86 Obesity http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12031976&form=6&db=m Altered tumor necrosis factor-alpha (TNF-alpha) processing in adipocytes and increased expression of transmembrane TNF-alpha in obesity. causal interaction,unassigned 4,0 3.4.24.86 Obesity http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19154693&form=6&db=m [The two sides of ADAM17 in inflammation: implications in atherosclerosis and obesity] causal interaction,therapeutic application,unassigned 4,1,0 3.4.24.86 Obesity http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19819120&form=6&db=m ADAM17_i33708A>G polymorphism interacts with dietary n-6 polyunsaturated fatty acids to modulate obesity risk in the Genetics of Lipid Lowering Drugs and Diet Network study. causal interaction,diagnostic usage,ongoing research,unassigned 4,2,2,0 3.4.24.86 Obesity http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28473444&form=6&db=m Role of Adipose Tissue Endothelial ADAM17 in Age-Related Coronary Microvascular Dysfunction. causal interaction,ongoing research,therapeutic application,unassigned 3,2,1,0 3.4.24.86 Obesity http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32184787&form=6&db=m Dendritic Cell-Restricted Progenitors Contribute to Obesity-Associated Airway Inflammation via Adam17-p38 MAPK-Dependent Pathway. causal interaction,unassigned 4,0 3.4.24.86 Obesity http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33330676&form=6&db=m The Role of iRhom2 in Metabolic and Cardiovascular-Related Disorders. causal interaction,therapeutic application,unassigned 4,1,0 3.4.24.86 Obesity http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33904577&form=6&db=m Implications of ADAM17 activation for hyperglycaemia, obesity and type 2 diabetes. causal interaction,ongoing research,therapeutic application,unassigned 3,2,4,0 3.4.24.86 Osteoarthritis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9574564&form=6&db=m TNF-alpha convertase enzyme from human arthritis-affected cartilage: isolation of cDNA by differential display, expression of the active enzyme, and regulation of TNF-alpha. unassigned - 3.4.24.86 Osteoarthritis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=14579524&form=6&db=m Design strategies for the identification of MMP-13 and Tace inhibitors. causal interaction,therapeutic application,unassigned 4,4,0 3.4.24.86 Osteoarthritis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30071898&form=6&db=m ADAM-17 is expressed on rheumatoid arthritis fibroblast-like synoviocytes and regulates proinflammatory mediator expression and monocyte adhesion. causal interaction,diagnostic usage,ongoing research,unassigned 2,4,4,0 3.4.24.86 Osteosarcoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29923217&form=6&db=m Expression of the ectodomain-releasing protease ADAM17 is directly regulated by the osteosarcoma and bone-related transcription factor RUNX2. causal interaction,diagnostic usage,unassigned 4,3,0 3.4.24.86 Ovarian Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16000554&form=6&db=m Lysophosphatidic acid, a disintegrin and metalloprotease-17 and heparin-binding epidermal growth factor-like growth factor in ovarian cancer: the first word, not the last. causal interaction,diagnostic usage,ongoing research,unassigned 1,1,3,0 3.4.24.86 Ovarian Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16000575&form=6&db=m Clinical significance of heparin-binding epidermal growth factor-like growth factor and a disintegrin and metalloprotease 17 expression in human ovarian cancer. causal interaction,diagnostic usage,ongoing research,unassigned 1,3,3,0 3.4.24.86 Ovarian Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21175594&form=6&db=m ADAM metallopeptidase domain 17 (ADAM17) is naturally processed through major histocompatibility complex (MHC) class I molecules and is a potential immunotherapeutic target in breast, ovarian and prostate cancers. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,4,4 3.4.24.86 Ovarian Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24044434&form=6&db=m Selective Arylsulfonamide Inhibitors of ADAM-17: Hit Optimization and Activity in Ovarian Cancer Cell Models. therapeutic application,unassigned 4,0 3.4.24.86 Ovarian Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28232483&form=6&db=m Ectodomain shedding of the cell adhesion molecule Nectin-4 in ovarian cancer is mediated by ADAM10 and ADAM17. ongoing research,unassigned 1,0 3.4.24.86 Ovarian Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28387913&form=6&db=m Nivolumab effectively inhibit platinum-resistant ovarian cancer cells via induction of cell apoptosis and inhibition of ADAM17 expression. causal interaction,ongoing research,therapeutic application,unassigned 1,3,2,0 3.4.24.86 Ovarian Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29662625&form=6&db=m ADAM17 inhibition enhances platinum efficiency in ovarian cancer. causal interaction,diagnostic usage,ongoing research,therapeutic application 2,1,2,4 3.4.24.86 Ovarian Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30065191&form=6&db=m Bisphenol-A and Nonylphenol Induce Apoptosis in Reproductive Tract Cancer Cell Lines by the Activation of ADAM17. ongoing research,therapeutic application,unassigned 3,4,0 3.4.24.86 Ovarian Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30904547&form=6&db=m Metalloproteinases at the surface of small extrcellular vesicles in advanced ovarian cancer: Relationships with ascites volume and peritoneal canceromatosis index. diagnostic usage,ongoing research,unassigned 4,3,0 3.4.24.86 Ovarian Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32851734&form=6&db=m Lysophosphatidic acid induces tumor necrosis factor-alpha to regulate a pro-inflammatory cytokine network in ovarian cancer. causal interaction,diagnostic usage,therapeutic application,unassigned 2,1,1,0 3.4.24.86 Ovarian Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33922533&form=6&db=m ADAM17 Inhibition Increases the Impact of Cisplatin Treatment in Ovarian Cancer Spheroids. causal interaction,ongoing research,therapeutic application,unassigned 4,4,4,0 3.4.24.86 Pancreatic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19603023&form=6&db=m Increased expression of ALCAM/CD166 in pancreatic cancer is an independent prognostic marker for poor survival and early tumour relapse. causal interaction,diagnostic usage,ongoing research,therapeutic application 1,2,3,1 3.4.24.86 Pancreatic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22509934&form=6&db=m A novel bispecific single-chain antibody for ADAM17 and CD3 induces T-cell-mediated lysis of prostate cancer cells. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,3,4,1 3.4.24.86 Pancreatic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29464088&form=6&db=m Deciphering microRNA targets in pancreatic cancer using miRComb R package. causal interaction,unassigned 2,0 3.4.24.86 Parkinson Disease http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30941646&form=6&db=m Genetic Association Between NGFR, ADAM17 Gene Polymorphism, and Parkinson's Disease in the Chinese Han Population. causal interaction,ongoing research,unassigned 1,1,0 3.4.24.86 Pemphigoid, Bullous http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22713436&form=6&db=m Does Adam17 cause the destruction of anchoring fibers via shedding tumor necrosis factor ? in bullous pemphigoid and dermatitis herpetiformis? unassigned - 3.4.24.86 Peptic Ulcer http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29434796&form=6&db=m ADAM proteases involved in inflammation are differentially altered in patients with gastritis or ulcer. causal interaction,diagnostic usage,ongoing research,unassigned 4,4,3,0 3.4.24.86 Periodontal Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18296613&form=6&db=m Tumor necrosis factor-alpha-converting enzyme (TACE) levels in periodontal diseases. diagnostic usage,unassigned 1,0 3.4.24.86 Periodontal Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23360525&form=6&db=m Periodontal disease and gene-expression levels of metalloendopeptidases in human buccal mucosal epithelium. causal interaction,diagnostic usage,ongoing research,unassigned 4,3,3,0 3.4.24.86 Periodontal Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28637950&form=6&db=m ADAM17 regulates TNF-? expression upon lipopolysaccharide stimulation in oral keratinocytes. causal interaction,unassigned 3,0 3.4.24.86 Periodontitis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23360525&form=6&db=m Periodontal disease and gene-expression levels of metalloendopeptidases in human buccal mucosal epithelium. causal interaction,diagnostic usage,ongoing research,unassigned 4,3,3,0 3.4.24.86 Peritonitis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15942356&form=6&db=m Regulation of peritoneal and systemic neutrophil-derived tumor necrosis factor-alpha release in patients with severe peritonitis: role of tumor necrosis factor-alpha converting enzyme cleavage. ongoing research,unassigned 1,0 3.4.24.86 Peritonitis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15942388&form=6&db=m Caught in the act: observation of polymorphonuclear neutrophils for the regulation of tumor necrosis factor-alpha release by tumor necrosis factor-alpha converting enzyme in patients with secondary peritonitis. unassigned - 3.4.24.86 Peritonitis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20154226&form=6&db=m In vivo role of leukocyte ADAM17 in the inflammatory and host responses during E. coli-mediated peritonitis. causal interaction,ongoing research,therapeutic application,unassigned 4,2,1,0 3.4.24.86 Peritonitis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29891514&form=6&db=m Neutrophil and macrophage cell surface CSF-1 shed by ADAM17 drives mouse macrophage proliferation in acute and chronic inflammation. ongoing research,unassigned 4,0 3.4.24.86 Pneumonia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12447765&form=6&db=m Tumor necrosis factor-alpha-converting enzyme: its role in community-acquired pneumonia. unassigned - 3.4.24.86 Pneumonia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21603616&form=6&db=m Leukocyte ADAM17 regulates acute pulmonary inflammation. causal interaction,ongoing research,therapeutic application,unassigned 4,4,3,0 3.4.24.86 Pneumonia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22367719&form=6&db=m Lung endothelial ADAM17 regulates the acute inflammatory response to lipopolysaccharide. diagnostic usage,unassigned 3,0 3.4.24.86 Pneumonia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24833351&form=6&db=m Leukocytes require ADAM10 but not ADAM17 for their migration and inflammatory recruitment into the alveolar space. causal interaction,ongoing research,unassigned 1,4,0 3.4.24.86 Pneumonia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33181031&form=6&db=m ADAM17 Deficiency Protects against Pulmonary Emphysema. causal interaction,ongoing research,therapeutic application,unassigned 4,3,4,0 3.4.24.86 Pneumonia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34051616&form=6&db=m Abnormal ADAM17 expression causes airway fibrosis in chronic obstructive asthma. causal interaction,unassigned 4,0 3.4.24.86 Pneumonia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34306143&form=6&db=m Examining the Effector Mechanisms of the Feishu Acupoint (BL13) in the Treatment of Pneumonia Based on Systematic Acupuncture and Moxibustion Research. therapeutic application,unassigned 1,0 3.4.24.86 Polycystic Kidney Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11576338&form=6&db=m A novel inhibitor of tumor necrosis factor-alpha converting enzyme ameliorates polycystic kidney disease. causal interaction,ongoing research,therapeutic application,unassigned 2,2,4,0 3.4.24.86 Polycystic Kidney Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15774823&form=6&db=m Transforming growth factor alpha (TGF-alpha) and other targets of tumor necrosis factor-alpha converting enzyme (TACE) in murine polycystic kidney disease. causal interaction,diagnostic usage,ongoing research,therapeutic application 2,3,1,1 3.4.24.86 Polycystic Kidney Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22413019&form=6&db=m A Disintegrin and Metalloenzyme (ADAM) 17 Activation Is Regulated by ?5?1 Integrin in Kidney Mesangial Cells. unassigned - 3.4.24.86 Polycystic Kidney Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24899059&form=6&db=m ADAM17 promotes proliferation of collecting duct kidney epithelial cells through ERK activation and increased glycolysis in polycystic kidney disease. causal interaction,diagnostic usage,ongoing research,unassigned 1,3,4,0 3.4.24.86 Polycystic Kidney, Autosomal Recessive http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11576338&form=6&db=m A novel inhibitor of tumor necrosis factor-alpha converting enzyme ameliorates polycystic kidney disease. causal interaction,ongoing research,therapeutic application,unassigned 2,2,4,0 3.4.24.86 Polymyositis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17207628&form=6&db=m The cell-specific expression of metalloproteinase-disintegrins (ADAMs) in inflammatory myopathies. diagnostic usage,ongoing research,therapeutic application,unassigned 3,4,2,0 3.4.24.86 Porcine Reproductive and Respiratory Syndrome http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24965453&form=6&db=m Modulation of CD163 expression by metalloprotease ADAM17 regulates porcine reproductive and respiratory syndrome virus entry. causal interaction,ongoing research,unassigned 4,1,0 3.4.24.86 Porcine Reproductive and Respiratory Syndrome http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27174637&form=6&db=m Correction for Guo et al., Modulation of CD163 Expression by Metalloprotease ADAM17 Regulates Porcine Reproductive and Respiratory Syndrome Virus Entry. unassigned - 3.4.24.86 Primary Dysautonomias http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31006330&form=6&db=m Activation of ADAM17 (A Disintegrin and Metalloprotease 17) on Glutamatergic Neurons Selectively Promotes Sympathoexcitation. causal interaction,diagnostic usage,ongoing research,therapeutic application 2,2,4,1 3.4.24.86 Prostatic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21175594&form=6&db=m ADAM metallopeptidase domain 17 (ADAM17) is naturally processed through major histocompatibility complex (MHC) class I molecules and is a potential immunotherapeutic target in breast, ovarian and prostate cancers. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,4,4 3.4.24.86 Prostatic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21837402&form=6&db=m ADAM17 regulates prostate cancer cell proliferation through mediating cell cycle progression by EGFR/PI3K/AKT pathway. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,4,1 3.4.24.86 Prostatic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22200661&form=6&db=m ADAM17 targets MMP-2 and MMP-9 via EGFR-MEK-ERK pathway activation to promote prostate cancer cell invasion. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,4,3 3.4.24.86 Prostatic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22509934&form=6&db=m A novel bispecific single-chain antibody for ADAM17 and CD3 induces T-cell-mediated lysis of prostate cancer cells. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,3,4,1 3.4.24.86 Prostatic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22934512&form=6&db=m [Inhibitory effect of siRNA targeting ADAM17 on the proliferation of prostate cancer PC-3 cells]. ongoing research,unassigned 4,0 3.4.24.86 Prostatic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24385212&form=6&db=m ALCAM/CD166 Is a TGF-?-Responsive Marker and Functional Regulator of Prostate Cancer Metastasis to Bone. ongoing research,unassigned 3,0 3.4.24.86 Prostatic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27941799&form=6&db=m Inhibition of Notch pathway arrests PTEN-deficient advanced prostate cancer by triggering p27-driven cellular senescence. causal interaction,therapeutic application,unassigned 4,4,0 3.4.24.86 Prostatic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33204367&form=6&db=m CD82 Suppresses ADAM17-Dependent E-Cadherin Cleavage and Cell Migration in Prostate Cancer. therapeutic application,unassigned 1,0 3.4.24.86 Proteinuria http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26697977&form=6&db=m Paricalcitol modulates ACE2 shedding and renal ADAM17 in NOD mice beyond proteinuria. ongoing research,unassigned 3,0 3.4.24.86 Psoriasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20070837&form=6&db=m Tumor necrosis factor-alpha-converting enzyme as a potential mediator of the influence of smoking on the response to treatment with narrowband ultraviolet B in psoriasis patients. causal interaction,therapeutic application,unassigned 1,4,0 3.4.24.86 Pulmonary Arterial Hypertension http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32762876&form=6&db=m Lung ACE2 and ADAM17 in pulmonary arterial hypertension: Implications for COVID-19? causal interaction,therapeutic application,unassigned 2,2,0 3.4.24.86 Pulmonary Disease, Chronic Obstructive http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17908459&form=6&db=m Expressions of tumor necrosis factor-converting enzyme and ErbB3 in rats with chronic obstructive pulmonary disease. causal interaction,ongoing research,therapeutic application,unassigned 4,3,1,0 3.4.24.86 Pulmonary Disease, Chronic Obstructive http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21861887&form=6&db=m Role of aberrant metalloproteinase activity in the pro-inflammatory phenotype of bronchial epithelium in COPD. causal interaction,ongoing research,unassigned 3,4,0 3.4.24.86 Pulmonary Disease, Chronic Obstructive http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27561911&form=6&db=m ADAM17 and EGFR regulate IL-6 receptor and amphiregulin mRNA expression and release in cigarette smoke-exposed primary bronchial epithelial cells from patients with chronic obstructive pulmonary disease (COPD). causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,4,1 3.4.24.86 Pulmonary Disease, Chronic Obstructive http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33181031&form=6&db=m ADAM17 Deficiency Protects against Pulmonary Emphysema. causal interaction,ongoing research,therapeutic application,unassigned 4,3,4,0 3.4.24.86 Pulmonary Emphysema http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32130031&form=6&db=m ADAM17 protects against elastase-induced emphysema by suppressing CD62L+ leukocyte infiltration in mice. causal interaction,therapeutic application,unassigned 3,4,0 3.4.24.86 Pulmonary Emphysema http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33181031&form=6&db=m ADAM17 Deficiency Protects against Pulmonary Emphysema. causal interaction,ongoing research,therapeutic application,unassigned 4,3,4,0 3.4.24.86 Pulmonary Fibrosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29902535&form=6&db=m ADAM17/EGFR-dependent ERK activation mediates thrombin-induced CTGF expression in human lung fibroblasts. causal interaction,unassigned 4,0 3.4.24.86 Renal Insufficiency, Chronic http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20566668&form=6&db=m Bradykinin decreases podocyte permeability through ADAM17-dependent epidermal growth factor receptor activation and zonula occludens-1 rearrangement. causal interaction,therapeutic application,unassigned 4,4,0 3.4.24.86 Renal Insufficiency, Chronic http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22413019&form=6&db=m A Disintegrin and Metalloenzyme (ADAM) 17 Activation Is Regulated by ?5?1 Integrin in Kidney Mesangial Cells. unassigned - 3.4.24.86 Renal Insufficiency, Chronic http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27642633&form=6&db=m ADAM17 substrate release in proximal tubule drives kidney fibrosis. unassigned - 3.4.24.86 Renal Insufficiency, Chronic http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29369823&form=6&db=m iRhom2 promotes lupus nephritis through TNF-? and EGFR signaling. causal interaction,unassigned 3,0 3.4.24.86 Renal Insufficiency, Chronic http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31141400&form=6&db=m Role of ADAM17 in kidney disease. causal interaction,ongoing research,therapeutic application,unassigned 4,3,4,0 3.4.24.86 Reperfusion Injury http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17619015&form=6&db=m Effects of PKF242-484 and PKF241-466, novel dual inhibitors of TNF-alpha converting enzyme and matrix metalloproteinases, in a model of intestinal reperfusion injury in mice. ongoing research,therapeutic application,unassigned 2,4,0 3.4.24.86 Reperfusion Injury http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31676723&form=6&db=m Proximal Tubule-Derived Amphiregulin Amplifies and Integrates Profibrotic EGF Receptor Signals in Kidney Fibrosis. causal interaction,diagnostic usage,ongoing research,therapeutic application 1,3,3,1 3.4.24.86 Reperfusion Injury http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33275250&form=6&db=m Influences of miR-708 on cerebral ischemia-reperfusion injury through targeted regulation of ADAM17. causal interaction,ongoing research,therapeutic application,unassigned 4,1,1,0 3.4.24.86 Retinal Neovascularization http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20110534&form=6&db=m Pathological neovascularization is reduced by inactivation of ADAM17 in endothelial cells but not in pericytes. diagnostic usage,ongoing research,unassigned 3,4,0 3.4.24.86 Retinal Neovascularization http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23299479&form=6&db=m Intravitreal injection of TIMP3 or the EGFR inhibitor erlotinib offers protection from oxygen-induced retinopathy in mice. therapeutic application,unassigned 2,0 3.4.24.86 Rhinitis, Allergic http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26250527&form=6&db=m Expression profile of ADAM10 and ADAM17 in allergic rhinitis. causal interaction,diagnostic usage,ongoing research,unassigned 4,3,4,0 3.4.24.86 Sarcoma, Synovial http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30627328&form=6&db=m Analysis of mutations in primary and metastatic synovial sarcoma. ongoing research,unassigned 4,0 3.4.24.86 Seizures http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15145598&form=6&db=m In pneumococcal meningitis a novel water-soluble inhibitor of matrix metalloproteinases and TNF-alpha converting enzyme attenuates seizures and injury of the cerebral cortex. therapeutic application,unassigned 3,0 3.4.24.86 Sepsis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12061836&form=6&db=m Differential effects between marimastat, a TNF-alpha converting enzyme inhibitor, and anti-TNF-alpha antibody on murine models for sepsis and arthritis. ongoing research,therapeutic application,unassigned 4,2,0 3.4.24.86 Sepsis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23757215&form=6&db=m TNF? cleavage beyond TACE/ADAM17: matrix metalloproteinase 13 is a potential therapeutic target in sepsis and colitis. causal interaction,therapeutic application,unassigned 2,4,0 3.4.24.86 Sepsis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27059842&form=6&db=m Targeting ADAM17 in leukocytes increases neutrophil recruitment and reduces bacterial spread during polymicrobial sepsis. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,2,1 3.4.24.86 Sepsis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27607600&form=6&db=m Association Study Between Promoter Polymorphisms of ADAM17 and Progression of Sepsis. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,2,1,1 3.4.24.86 Sepsis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28487846&form=6&db=m Ectodomain Shedding by ADAM17: Its Role in Neutrophil Recruitment and the Impairment of This Process during Sepsis. causal interaction,ongoing research,therapeutic application,unassigned 3,2,1,0 3.4.24.86 Sepsis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32932701&form=6&db=m Blocking ADAM17 Function with a Monoclonal Antibody Improves Sepsis Survival in a Murine Model of Polymicrobial Sepsis. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,2,4,4 3.4.24.86 Severe Acute Respiratory Syndrome http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21563828&form=6&db=m Angiotensin-converting enzyme 2 ectodomain shedding cleavage-site identification: determinants and constraints. causal interaction,diagnostic usage,unassigned 4,1,0 3.4.24.86 Severe Acute Respiratory Syndrome http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24227843&form=6&db=m TMPRSS2 and ADAM17 cleave ACE2 differentially and only proteolysis by TMPRSS2 augments entry driven by the severe acute respiratory syndrome coronavirus spike protein. therapeutic application,unassigned 1,0 3.4.24.86 Severe Acute Respiratory Syndrome http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32769398&form=6&db=m Shedding Light on COVID-19: ADAM17 the Missing Link? causal interaction,diagnostic usage,ongoing research,therapeutic application 3,1,1,4 3.4.24.86 Severe Acute Respiratory Syndrome http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32783758&form=6&db=m ACE2 (Angiotensin-Converting Enzyme 2) in Cardiopulmonary Diseases: Ramifications for the Control of SARS-CoV-2. causal interaction,ongoing research,unassigned 4,2,0 3.4.24.86 Severe Acute Respiratory Syndrome http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34414454&form=6&db=m MicroRNA?28?3p inhibits angiotensin?converting enzyme 2 ectodomain shedding in 293T cells treated with the spike protein of severe acute respiratory syndrome coronavirus 2 by targeting A disintegrin and metalloproteinase 17. therapeutic application,unassigned 1,0 3.4.24.86 Shock, Septic http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20603312&form=6&db=m Critical role of the disintegrin metalloprotease ADAM17 for intestinal inflammation and regeneration in mice. causal interaction,diagnostic usage,ongoing research,unassigned 4,1,1,0 3.4.24.86 Shock, Septic http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22833676&form=6&db=m A disintegrin and metalloproteinase 17 (ADAM17) and epidermal growth factor receptor (EGFR) signaling drive the epithelial response to Staphylococcus aureus toxic shock syndrome toxin-1 (TSST-1). causal interaction,ongoing research,unassigned 3,2,0 3.4.24.86 Shock, Septic http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26373631&form=6&db=m Plasma soluble Tim-3 emerges as an inhibitor in sepsis: sepsis contrary to membrane Tim-3 on monocytes. unassigned - 3.4.24.86 Skin Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22772468&form=6&db=m Differentiation-induced skin cancer suppression by FOS, p53, and TACE/ADAM17. therapeutic application,unassigned 1,0 3.4.24.86 Spinal Cord Injuries http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24336074&form=6&db=m ADAM17 is a survival factor for microglial cells in vitro and in vivo after spinal cord injury in mice. causal interaction,ongoing research,unassigned 1,3,0 3.4.24.86 Spinal Cord Injuries http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25738567&form=6&db=m A disintegrin and metalloprotease 17 promotes microglial cell survival via epidermal growth factor receptor signalling following spinal cord injury. unassigned - 3.4.24.86 Spinal Cord Injuries http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30851378&form=6&db=m ADAM17-deficiency on microglia but not on macrophages promotes phagocytosis and functional recovery after spinal cord injury. causal interaction,therapeutic application,unassigned 3,1,0 3.4.24.86 Squamous Cell Carcinoma of Head and Neck http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17180679&form=6&db=m ADAM-17 associated with CD44 cleavage and metastasis in oral squamous cell carcinoma. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,2,4,1 3.4.24.86 Squamous Cell Carcinoma of Head and Neck http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17999917&form=6&db=m Involvement of NF-kappaB-mediated maturation of ADAM-17 in the invasion of oral squamous cell carcinoma. causal interaction,ongoing research,unassigned 3,3,0 3.4.24.86 Squamous Cell Carcinoma of Head and Neck http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24403253&form=6&db=m ADAM17-mediated CD44 cleavage promotes orasphere formation or stemness and tumorigenesis in HNSCC. causal interaction,diagnostic usage,ongoing research,therapeutic application 1,4,4,1 3.4.24.86 Squamous Cell Carcinoma of Head and Neck http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24495306&form=6&db=m ADAM17 mediates OSCC development in an orthotopic murine model. causal interaction,unassigned 4,0 3.4.24.86 Squamous Cell Carcinoma of Head and Neck http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25013379&form=6&db=m Targeting the sheddase activity of ADAM17 by an anti-ADAM17 antibody D1(A12) inhibits head and neck squamous cell carcinoma cell proliferation and motility via blockage of bradykinin induced HERs transactivation. causal interaction,ongoing research,therapeutic application,unassigned 4,4,4,0 3.4.24.86 Squamous Cell Carcinoma of Head and Neck http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27576135&form=6&db=m Mass spectrometry-based proteomics revealed Glypican-1 as a novel ADAM17 substrate. causal interaction,ongoing research,therapeutic application,unassigned 4,1,2,0 3.4.24.86 Squamous Cell Carcinoma of Head and Neck http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29171106&form=6&db=m Autophagy regulates cisplatin-induced stemness and chemoresistance via the upregulation of CD44, ABCB1 and ADAM17 in oral squamous cell carcinoma. causal interaction,diagnostic usage,unassigned 3,2,0 3.4.24.86 Squamous Cell Carcinoma of Head and Neck http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31207072&form=6&db=m MicroRNA-224, negatively regulated by c-jun, inhibits growth and epithelial-to-mesenchymal transition phenotype via targeting ADAM17 in oral squamous cell carcinoma. unassigned - 3.4.24.86 Stomach Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20934403&form=6&db=m TGF? induces proHB-EGF shedding and EGFR transactivation through ADAM activation in gastric cancer cells. unassigned - 3.4.24.86 Stomach Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21435459&form=6&db=m Genotypic and phenotypic characterization of side population of gastric cancer cell lines. causal interaction,unassigned 3,0 3.4.24.86 Stomach Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22139867&form=6&db=m Prognostic value of ADAM17 in human gastric cancer. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,4,3 3.4.24.86 Stomach Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22668812&form=6&db=m Upregulated Expression of ADAM17 Is a Prognostic Marker for Patients With Gastric Cancer. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,4,1 3.4.24.86 Stomach Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25499189&form=6&db=m Epithelial cell ADAM17 activation by Helicobacter pylori: role of ADAM17 C-terminus and Threonine-735 phosphorylation. therapeutic application,unassigned 4,0 3.4.24.86 Stomach Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25786367&form=6&db=m Prognostic significance of ADAM17 expression in patients with gastric cancer who underwent curative gastrectomy. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,4,2 3.4.24.86 Stomach Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26617808&form=6&db=m MiR-338-3p inhibits the proliferation and migration of gastric cancer cells by targeting ADAM17. causal interaction,diagnostic usage,ongoing research,unassigned 4,4,3,0 3.4.24.86 Stomach Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27779657&form=6&db=m ADAM17 promotes epithelial-mesenchymal transition via TGF-?/Smad pathway in gastric carcinoma cells. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,1,2,4 3.4.24.86 Stomach Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27878499&form=6&db=m Therapeutic potential of ADAM17 modulation in gastric cancer through regulation of the EGFR and TNF-? signalling pathways. causal interaction,diagnostic usage,ongoing research,unassigned 4,3,4,0 3.4.24.86 Stomach Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29180185&form=6&db=m ADAM-17 expression is enhanced by FoxM1 and is a poor prognostic sign in gastric carcinoma. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,3,3 3.4.24.86 Stomach Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30569104&form=6&db=m ADAM17 promotes lymph node metastasis in gastric cancer via activation of the Notch and Wnt signaling pathways. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,3,1 3.4.24.86 Stomach Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32610677&form=6&db=m Prognostic Significance of ADAM17 for Gastric Cancer Survival: A Meta-Analysis. causal interaction,diagnostic usage,therapeutic application,unassigned 4,4,3,0 3.4.24.86 Stomach Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33335725&form=6&db=m Luteolin alters MUC1 extracellular domain, sT antigen, ADAM-17, IL-8, IL-10 and NF-?B expression in Helicobacter pylori-infected gastric cancer CRL-1739 cells: A preliminary study. ongoing research,unassigned 4,0 3.4.24.86 Stroke http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17355261&form=6&db=m Inhibition of ADAM17 reduces hypoxia-induced brain tumor cell invasiveness. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,4,4 3.4.24.86 Stroke http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19223914&form=6&db=m Niaspan treatment increases tumor necrosis factor-alpha-converting enzyme and promotes arteriogenesis after stroke. ongoing research,therapeutic application,unassigned 1,4,0 3.4.24.86 Stroke http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19395875&form=6&db=m ADAM17 promotes breast cancer cell malignant phenotype through EGFR-PI3K-AKT activation. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,3,4,1 3.4.24.86 Stroke http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21480393&form=6&db=m ADAM17 promotes glioma cell malignant phenotype. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,4,1 3.4.24.86 Stroke http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23771674&form=6&db=m Changes in platelet GPIb? and ADAM17 during the acute stage of atherosclerotic ischemic stroke among Chinese. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,2,3,4 3.4.24.86 Stroke http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24727681&form=6&db=m Association between ADAM17 Promoter Polymorphisms and Ischemic Stroke in a Chinese Population. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,2,3,1 3.4.24.86 Stroke http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29021532&form=6&db=m Monocyte-lymphocyte cross-communication via soluble CD163 directly links innate immune system activation and adaptive immune system suppression following ischemic stroke. diagnostic usage,unassigned 4,0 3.4.24.86 Telangiectasia, Hereditary Hemorrhagic http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24812125&form=6&db=m Genetic variants of Adam17 differentially regulate TGF? signaling to modify vascular pathology in mice and humans. ongoing research,therapeutic application,unassigned 2,1,0 3.4.24.86 Telangiectasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24812125&form=6&db=m Genetic variants of Adam17 differentially regulate TGF? signaling to modify vascular pathology in mice and humans. ongoing research,therapeutic application,unassigned 2,1,0 3.4.24.86 Tetralogy of Fallot http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32103528&form=6&db=m Substrate-selective protein ectodomain shedding by ADAM17 and iRhom2 depends on their juxtamembrane and transmembrane domains. unassigned - 3.4.24.86 Thrombosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33979555&form=6&db=m Actin polymerization regulates glycoprotein Ib? shedding. unassigned - 3.4.24.86 Thrombosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34419773&form=6&db=m Which ones, when and why should renin-angiotensin system inhibitors work against COVID-19? causal interaction,unassigned 3,0 3.4.24.86 Thyroid Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21779480&form=6&db=m The Putative PAX8/PPAR? Fusion Oncoprotein Exhibits Partial Tumor Suppressor Activity through Up-Regulation of Micro-RNA-122 and Dominant-Negative PPAR? Activity. causal interaction,unassigned 3,0 3.4.24.86 Thyroiditis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32204685&form=6&db=m Elevated MicroRNA-326 Levels Regulate the IL-23/IL-23R/Th17 Cell Axis in Hashimoto's Thyroiditis by Targeting a Disintegrin and Metalloprotease 17. diagnostic usage,unassigned 1,0 3.4.24.86 Tics http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23548270&form=6&db=m miR145 targets the SOX9/ADAM17 axis to inhibit tumor-initiating cells and IL-6-mediated paracrine effects in head and neck cancer. therapeutic application,unassigned 1,0 3.4.24.86 Trauma, Nervous System http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30851378&form=6&db=m ADAM17-deficiency on microglia but not on macrophages promotes phagocytosis and functional recovery after spinal cord injury. causal interaction,therapeutic application,unassigned 3,1,0 3.4.24.86 Triple Negative Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22967992&form=6&db=m ADAM-17: a novel therapeutic target for triple negative breast cancer. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,2,4,4 3.4.24.86 Triple Negative Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26010411&form=6&db=m Targeting ADAM-17 with an inhibitory monoclonal antibody has antitumour effects in triple-negative breast cancer cells. ongoing research,therapeutic application,unassigned 3,3,0 3.4.24.86 Triple Negative Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31796994&form=6&db=m Proteolytic processing of PD-L1 by ADAM proteases in breast cancer cells. diagnostic usage,ongoing research,therapeutic application,unassigned 3,1,1,0 3.4.24.86 Triple Negative Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32927582&form=6&db=m ADAM-17: a novel therapeutic target for triple negative breast cancer. causal interaction,therapeutic application,unassigned 3,4,0 3.4.24.86 Uremia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29056164&form=6&db=m ADAM17, a New Player in the Pathogenesis of Chronic Kidney Disease-Mineral and Bone Disorder. causal interaction,diagnostic usage,ongoing research,unassigned 4,2,2,0 3.4.24.86 Uterine Cervical Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24793016&form=6&db=m ADAM17 is associated with EMMPRIN and predicts poor prognosis in patients with uterine cervical carcinoma. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,4,4,3 3.4.24.86 Uterine Cervical Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30603978&form=6&db=m Nanoquinacrine sensitizes 5-FU-resistant cervical cancer stem-like cells by down-regulating Nectin-4 via ADAM-17 mediated NOTCH deregulation. unassigned - 3.4.24.86 Vascular Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24812125&form=6&db=m Genetic variants of Adam17 differentially regulate TGF? signaling to modify vascular pathology in mice and humans. ongoing research,therapeutic application,unassigned 2,1,0 3.4.24.86 Vascular System Injuries http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21357274&form=6&db=m A disintegrin and metalloprotease 17 mediates neointimal hyperplasia in vasculature. causal interaction,unassigned 4,0 3.4.24.86 Ventilator-Induced Lung Injury http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25085885&form=6&db=m Hypercapnia attenuates ventilator-induced lung injury via a disintegrin and metalloprotease-17. causal interaction,ongoing research,therapeutic application,unassigned 2,3,1,0 3.4.24.86 Virus Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29475600&form=6&db=m Metalloprotease ADAM17 regulates porcine epidemic diarrhea virus infection by modifying aminopeptidase N. causal interaction,ongoing research,therapeutic application,unassigned 3,2,2,0 3.4.24.86 Virus Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32385608&form=6&db=m Tetraspanin CD9 affects HPV16 infection by modulating ADAM17 activity and the ERK signalling pathway. therapeutic application,unassigned 1,0 3.4.24.86 Virus Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33519802&form=6&db=m Does Angiotensin II Peak in Response to SARS-CoV-2? ongoing research,therapeutic application,unassigned 2,1,0 3.4.24.86 Virus Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33684175&form=6&db=m ADAM17 is an essential attachment factor for classical swine fever virus. causal interaction,ongoing research,unassigned 3,1,0