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Disease on EC 3.4.24.B28 - ADAM15

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DISEASE
TITLE OF PUBLICATION
LINK TO PUBMED
Acute Lung Injury
ADAM15 deficiency attenuates pulmonary hyperpermeability and acute lung injury in lipopolysaccharide-treated mice.
adam15 deficiency
A disintegrin and metalloproteinase 15-mediated glycocalyx shedding contributes to vascular leakage during inflammation.
A disintegrin and metalloproteinase domain-15 deficiency leads to exaggerated cigarette smoke-induced chronic obstructive pulmonary disease (COPD)-like disease in mice.
ADAM (a Disintegrin and Metalloproteinase) 15 Deficiency Exacerbates Ang II (Angiotensin II)-Induced Aortic Remodeling Leading to Abdominal Aortic Aneurysm.
ADAM15 deficiency attenuates pulmonary hyperpermeability and acute lung injury in lipopolysaccharide-treated mice.
Homeostatic effects of the metalloproteinase disintegrin ADAM15 in degenerative cartilage remodeling.
Adenocarcinoma
ADAM15 disintegrin is associated with aggressive prostate and breast cancer disease.
ADAM15 is involved in MICB shedding and mediates the effects of gemcitabine on MICB shedding in PANC-1 pancreatic cancer cells.
Expression of ADAM15 in lung carcinomas.
Aneurysm
ADAM (a Disintegrin and Metalloproteinase) 15 Deficiency Exacerbates Ang II (Angiotensin II)-Induced Aortic Remodeling Leading to Abdominal Aortic Aneurysm.
Aortic Aneurysm, Abdominal
ADAM (a Disintegrin and Metalloproteinase) 15 Deficiency Exacerbates Ang II (Angiotensin II)-Induced Aortic Remodeling Leading to Abdominal Aortic Aneurysm.
Arthritis
A disintegrin and metallproteinase 15 knockout decreases migration of fibroblast-like synoviocytes and inflammation in rheumatoid arthritis.
Arthritis, Rheumatoid
A Disintegrin and Metalloprotease 15 is Expressed on Rheumatoid Arthritis Synovial Tissue Endothelial Cells and may Mediate Angiogenesis.
ADAM15 adds to apoptosis resistance of synovial fibroblasts by modulating focal adhesion kinase signaling.
ADAM15 in apoptosis resistance of synovial fibroblasts: converting Fas/CD95 death signals into the activation of pro-survival pathways by calmodulin recruitment.
Atherosclerosis
A Disintegrin and Metalloproteinase 15 Contributes to Atherosclerosis by Mediating Endothelial Barrier Dysfunction via Src Family Kinase Activity.
ADAM33 expression in atherosclerotic lesions and relationship of ADAM33 gene variation with atherosclerosis.
Loss of protease activity of ADAM15 abolishes protective effects on plaque progression in atherosclerosis.
Breast Neoplasms
Aberrant alternative exon use and increased copy number of human metalloprotease-disintegrin ADAM15 gene in breast cancer cells.
ADAM15 disintegrin is associated with aggressive prostate and breast cancer disease.
ADAM15 mediates upregulation of Claudin-1 expression in breast cancer cells.
ADAM15 participates in fertilization through a physical interaction with acrogranin.
ADAM22 as a prognostic and therapeutic drug target in the treatment of endocrine-resistant breast cancer.
Src stimulates fibroblast growth factor receptor-2 shedding by an ADAM15 splice variant linked to breast cancer.
The ectodomain shedding of E-cadherin by ADAM15 supports ErbB receptor activation.
Carcinoma
ADAM15 to ?5?1 integrin switch in colon carcinoma cells : A late event in cancer progression associated with tumor dedifferentiation and poor prognosis.
Expression of ADAM15 in lung carcinomas.
Carcinoma, Hepatocellular
ADAM15 correlates with prognosis, immune infiltration and apoptosis in hepatocellular carcinoma.
Carcinoma, Non-Small-Cell Lung
ADAM15 targets MMP9 activity to promote lung cancer cell invasion.
Cardiomyopathy, Dilated
Altered expression of disintegrin metalloproteinases and their inhibitor in human dilated cardiomyopathy.
Cartilage Diseases
ADAM15 MODULATES OUTSIDE-IN SIGNALING IN CHONDROCYTE-MATRIX INTERACTIONS.
Chondrosarcoma
Interleukin 13 (IL-13)-regulated expression of the chondroprotective metalloproteinase ADAM15 is reduced in aging cartilage.
Choroidal Neovascularization
An Adam15 amplification loop promotes vascular endothelial growth factor-induced ocular neovascularization.
Colitis, Ulcerative
ADAM15 upregulation and interaction with multiple binding partners in inflammatory bowel disease.
Colorectal Neoplasms
ADAM15 to ?5?1 integrin switch in colon carcinoma cells : A late event in cancer progression associated with tumor dedifferentiation and poor prognosis.
Crohn Disease
ADAM15 upregulation and interaction with multiple binding partners in inflammatory bowel disease.
Encephalitis, Tick-Borne
ADAM15 Participates in Tick-Borne Encephalitis Virus Replication.
Hypertension
ADAM (a Disintegrin and Metalloproteinase) 15 Deficiency Exacerbates Ang II (Angiotensin II)-Induced Aortic Remodeling Leading to Abdominal Aortic Aneurysm.
Immune System Diseases
ADAM15 deficiency attenuates pulmonary hyperpermeability and acute lung injury in lipopolysaccharide-treated mice.
Infections
ADAM15 Participates in Tick-Borne Encephalitis Virus Replication.
Inflammatory Bowel Diseases
ADAM15 to ?5?1 integrin switch in colon carcinoma cells : A late event in cancer progression associated with tumor dedifferentiation and poor prognosis.
ADAM15 upregulation and interaction with multiple binding partners in inflammatory bowel disease.
Liver Neoplasms
ADAM15 correlates with prognosis, immune infiltration and apoptosis in hepatocellular carcinoma.
Lung Injury
ADAM15 deficiency attenuates pulmonary hyperpermeability and acute lung injury in lipopolysaccharide-treated mice.
Lung Neoplasms
ADAM15 targets MMP9 activity to promote lung cancer cell invasion.
Lymphatic Metastasis
ADAM15 is involved in MICB shedding and mediates the effects of gemcitabine on MICB shedding in PANC-1 pancreatic cancer cells.
Melanoma
ADAM15 expression is downregulated in melanoma metastasis compared to primary melanoma.
Identification of binding peptides of the ADAM15 disintegrin domain using phage display.
NCK1-AS1 promotes the progression of melanoma by accelerating cell proliferation and migration via targeting miR-526b-5p/ADAM15 axis.
Screening cellular proteins involved in the anti-proliferative effect of the ADAM15 disintegrin domain in murine melanoma cells.
Neoplasm Metastasis
ADAM15 expression is downregulated in melanoma metastasis compared to primary melanoma.
ADAM15 is involved in MICB shedding and mediates the effects of gemcitabine on MICB shedding in PANC-1 pancreatic cancer cells.
ADAM15 supports prostate cancer metastasis by modulating tumor cell-endothelial cell interaction.
ADAM15 suppresses cell motility by driving integrin alpha5beta1 cell surface expression via Erk inactivation.
Characterization of the catalytic activity of the membrane-anchored metalloproteinase ADAM15 in cell-based assays.
Critical role of ADAM15 in tumor progression: targeting multiple factors for metastasis promotion.
Expression of ADAM15 in lung carcinomas.
MicroRNA miR-24 Enhances Tumor Invasion and Metastasis by Targeting PTPN9 and PTPRF to Promote EGF Signaling.
The role of the disintegrin metalloproteinase ADAM15 in prostate cancer progression.
Neoplasms
A Disintegrin and Metalloprotease 15 is Expressed on Rheumatoid Arthritis Synovial Tissue Endothelial Cells and may Mediate Angiogenesis.
Aberrant alternative exon use and increased copy number of human metalloprotease-disintegrin ADAM15 gene in breast cancer cells.
ADAM15 correlates with prognosis, immune infiltration and apoptosis in hepatocellular carcinoma.
ADAM15 decreases integrin alphavbeta3/vitronectin-mediated ovarian cancer cell adhesion and motility in an RGD-dependent fashion.
ADAM15 deficiency attenuates pulmonary hyperpermeability and acute lung injury in lipopolysaccharide-treated mice.
ADAM15 disintegrin is associated with aggressive prostate and breast cancer disease.
ADAM15 gene structure and differential alternative exon use in human tissues.
ADAM15 Is Functionally Associated with the Metastatic Progression of Human Bladder Cancer.
ADAM15 is involved in MICB shedding and mediates the effects of gemcitabine on MICB shedding in PANC-1 pancreatic cancer cells.
ADAM15 supports prostate cancer metastasis by modulating tumor cell-endothelial cell interaction.
ADAM15 targets MMP9 activity to promote lung cancer cell invasion.
ADAM15 to ?5?1 integrin switch in colon carcinoma cells : A late event in cancer progression associated with tumor dedifferentiation and poor prognosis.
ADAMs in cancer cell proliferation and progression.
Alternative splicing of ADAM15 regulates its interactions with cellular SH3 proteins.
Antitumor and anti-angiogenic activity of the recombinant human disintegrin domain of A disintegrin and metalloproteinase 15.
Cell adhesion-induced transient interaction of ADAM15 with poly(A) binding protein at the cell membrane colocalizes with mRNA translation.
Characterization of oxygen-induced retinopathy in mice carrying an inactivating point mutation in the catalytic site of ADAM15.
Characterization of the catalytic activity of the membrane-anchored metalloproteinase ADAM15 in cell-based assays.
Critical role of ADAM15 in tumor progression: targeting multiple factors for metastasis promotion.
Distinct ADAM metalloproteinases regulate G protein-coupled receptor-induced cell proliferation and survival.
Exosome release of ADAM15 and the functional implications of human macrophage-derived ADAM15 exosomes.
Expression of ADAM15 in lung carcinomas.
Expression of ADAM15 in rheumatoid synovium: up-regulation by vascular endothelial growth factor and possible implications for angiogenesis.
Identification of binding peptides of the ADAM15 disintegrin domain using phage display.
MicroRNA miR-24 Enhances Tumor Invasion and Metastasis by Targeting PTPN9 and PTPRF to Promote EGF Signaling.
Overexpression of the A Disintegrin and Metalloproteinase ADAM15 is linked to a Small but Highly Aggressive Subset of Prostate Cancers.
Recombinant disintegrin domain of ADAM15 inhibits the proliferation and migration of Bel-7402 cells.
The ADAM15 ectodomain is shed from secretory exosomes.
The ADAMs family of proteases: new biomarkers and therapeutic targets for cancer?
The microRNA miR-3174 Suppresses the Expression of ADAM15 and Inhibits the Proliferation of Patient-Derived Bladder Cancer Cells.
The role of the disintegrin metalloproteinase ADAM15 in prostate cancer progression.
The therapeutic potential of ADAM15.
Neoplasms, Squamous Cell
Expression of ADAM15 in lung carcinomas.
Neuroblastoma
ADAM15 Participates in Tick-Borne Encephalitis Virus Replication.
Nevus
ADAM15 expression is downregulated in melanoma metastasis compared to primary melanoma.
Osteoarthritis
ADAM15 MODULATES OUTSIDE-IN SIGNALING IN CHONDROCYTE-MATRIX INTERACTIONS.
Homeostatic effects of the metalloproteinase disintegrin ADAM15 in degenerative cartilage remodeling.
Interleukin 13 (IL-13)-regulated expression of the chondroprotective metalloproteinase ADAM15 is reduced in aging cartilage.
Ovarian Neoplasms
ADAM15 decreases integrin alphavbeta3/vitronectin-mediated ovarian cancer cell adhesion and motility in an RGD-dependent fashion.
The ADAM15 ectodomain is shed from secretory exosomes.
Pancreatic Neoplasms
ADAM15 is involved in MICB shedding and mediates the effects of gemcitabine on MICB shedding in PANC-1 pancreatic cancer cells.
Pneumonia
A disintegrin and metalloproteinase domain-15 deficiency leads to exaggerated cigarette smoke-induced chronic obstructive pulmonary disease (COPD)-like disease in mice.
ADAM-family metalloproteinases in lung inflammation: potential therapeutic targets.
Prostatic Neoplasms
ADAM15 disintegrin is associated with aggressive prostate and breast cancer disease.
ADAM15 supports prostate cancer metastasis by modulating tumor cell-endothelial cell interaction.
Characterization of the catalytic activity of the membrane-anchored metalloproteinase ADAM15 in cell-based assays.
EGF promotes the shedding of soluble E-cadherin in an ADAM10-dependent manner in prostate epithelial cells.
Overexpression of the A Disintegrin and Metalloproteinase ADAM15 is linked to a Small but Highly Aggressive Subset of Prostate Cancers.
The role of the disintegrin metalloproteinase ADAM15 in prostate cancer progression.
Pulmonary Disease, Chronic Obstructive
A disintegrin and metalloproteinase domain-15 deficiency leads to exaggerated cigarette smoke-induced chronic obstructive pulmonary disease (COPD)-like disease in mice.
ADAM15 expression is increased in lung CD8+ T cells, macrophages, and bronchial epithelial cells in patients with COPD and is inversely related to airflow obstruction.
Pulmonary Edema
ADAM15 deficiency attenuates pulmonary hyperpermeability and acute lung injury in lipopolysaccharide-treated mice.
Retinal Neovascularization
An Adam15 amplification loop promotes vascular endothelial growth factor-induced ocular neovascularization.
Sepsis
A disintegrin and metalloproteinase 15-mediated glycocalyx shedding contributes to vascular leakage during inflammation.
Starvation
Homeostatic effects of the metalloproteinase disintegrin ADAM15 in degenerative cartilage remodeling.
Status Epilepticus
ADAM9, ADAM10, and ADAM15 mRNA levels in the rat brain after kainic acid-induced status epilepticus.
Stomach Neoplasms
Expression of ADAM9 in CIN3 lesions and squamous cell carcinomas of the cervix.
The disintegrin-metalloproteinases ADAM9, ADAM12, and ADAM15 are upregulated in gastric cancer.
Thrombosis
ADAM 15 is an adhesion receptor for platelet GPIIb-IIIa and induces platelet activation.
Triple Negative Breast Neoplasms
Functional exosome-mediated co-delivery of doxorubicin and hydrophobically modified microRNA 159 for triple-negative breast cancer therapy.
Urinary Bladder Neoplasms
ADAM15 Is Functionally Associated with the Metastatic Progression of Human Bladder Cancer.
The microRNA miR-3174 Suppresses the Expression of ADAM15 and Inhibits the Proliferation of Patient-Derived Bladder Cancer Cells.
Urogenital Neoplasms
Distinct ADAM metalloproteinases regulate G protein-coupled receptor-induced cell proliferation and survival.
Vesicular Stomatitis
TRIF-mediated TLR3 and TLR4 signaling is negatively regulated by ADAM15.