2.4.1.94 Alzheimer Disease http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22314054&form=6&db=m O-GlcNAcase is essential for embryonic development and maintenance of genomic stability. unassigned - 2.4.1.94 Alzheimer Disease http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24144743&form=6&db=m [Effects of Xixin decoction on enzymes related to O-GlcNAc glycosylation of tau proteins in the brain of rats with sporadic Alzheimer's disease]. ongoing research,unassigned 2,0 2.4.1.94 Alzheimer Disease http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30237786&form=6&db=m Real Talk: The Inter-play Between the mTOR, AMPK, and Hexosamine Biosynthetic Pathways in Cell Signaling. causal interaction,unassigned 3,0 2.4.1.94 Alzheimer Disease http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32404505&form=6&db=m PET ligands [18F]LSN3316612 and [11C]LSN3316612 quantify O-linked-?-N-acetyl-glucosamine hydrolase in the brain. unassigned - 2.4.1.94 Aortic Valve Stenosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22128088&form=6&db=m Cardiac O-GlcNAc signaling is increased in hypertrophy and heart failure. ongoing research,unassigned 2,0 2.4.1.94 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20190804&form=6&db=m Nutrient sensor O-GlcNAc transferase regulates breast cancer tumorigenesis through targeting of the oncogenic transcription factor FoxM1. causal interaction,unassigned 3,0 2.4.1.94 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24214978&form=6&db=m O-GlcNAcylation of cofilin promotes breast cancer cell invasion. causal interaction,unassigned 4,0 2.4.1.94 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25636967&form=6&db=m mTOR/MYC Axis Regulates O-GlcNAc Transferase (OGT) Expression and O-GlcNAcylation in Breast Cancer. ongoing research,unassigned 2,0 2.4.1.94 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26374642&form=6&db=m Proteomic analysis of O-GlcNAcylated proteins in invasive ductal breast carcinomas with and without lymph node metastasis. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,3,2,1 2.4.1.94 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30952976&form=6&db=m O-GlcNAc Transferase Inhibition Differentially Affects Breast Cancer Subtypes. causal interaction,therapeutic application,unassigned 4,1,0 2.4.1.94 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31974291&form=6&db=m O-GlcNAc Transferase Regulates Cancer Stem-like Potential of Breast Cancer Cells. causal interaction,diagnostic usage,ongoing research,therapeutic application 2,1,1,2 2.4.1.94 Breast Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33046784&form=6&db=m Inhibition of O-GlcNAc transferase activates tumor-suppressor gene expression in tamoxifen-resistant breast cancer cells. diagnostic usage,ongoing research,therapeutic application,unassigned 1,3,1,0 2.4.1.94 Carcinogenesis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20190804&form=6&db=m Nutrient sensor O-GlcNAc transferase regulates breast cancer tumorigenesis through targeting of the oncogenic transcription factor FoxM1. causal interaction,unassigned 3,0 2.4.1.94 Carcinogenesis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29059153&form=6&db=m Nutrient sensor O-GlcNAc transferase controls cancer lipid metabolism via SREBP-1 regulation. causal interaction,therapeutic application,unassigned 3,1,0 2.4.1.94 Carcinogenesis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31933944&form=6&db=m Increased expression of O-GlcNAc transferase (OGT) is a biomarker for poor prognosis and allows tumorigenesis and invasion in colon cancer. causal interaction,diagnostic usage,unassigned 4,1,0 2.4.1.94 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22275356&form=6&db=m Critical role of O-GlcNAc transferase in prostate cancer invasion, angiogenesis and metastasis. causal interaction,diagnostic usage,ongoing research,unassigned 3,4,3,0 2.4.1.94 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33307156&form=6&db=m Exosomal O-GlcNAc transferase from esophageal carcinoma stem cell promotes cancer immunosuppression through up-regulation of PD-1 in CD8+ T cells. ongoing research,unassigned 2,0 2.4.1.94 Carcinoma, Hepatocellular http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28499244&form=6&db=m MicroRNA-24-1 suppresses mouse hepatoma cell invasion and metastasis via directly targeting O-GlcNAc transferase. causal interaction,diagnostic usage,unassigned 1,1,0 2.4.1.94 Carcinoma, Hepatocellular http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33121131&form=6&db=m O-GlcNAc Transferase Inhibitor Synergistically Enhances Doxorubicin-Induced Apoptosis in HepG2 Cells. causal interaction,therapeutic application,unassigned 3,4,0 2.4.1.94 Cardiovascular Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22314054&form=6&db=m O-GlcNAcase is essential for embryonic development and maintenance of genomic stability. unassigned - 2.4.1.94 Cardiovascular Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25495821&form=6&db=m The role of O-GlcNAc transferase in regulating the gene transcription of developing and failing hearts. causal interaction,unassigned 3,0 2.4.1.94 Cholangiocarcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23480751&form=6&db=m Overexpression of O-GlcNAc-Transferase Associates with Aggressiveness of Mass-Forming Cholangiocarcinoma. causal interaction,ongoing research,unassigned 1,3,0 2.4.1.94 Colonic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31933944&form=6&db=m Increased expression of O-GlcNAc transferase (OGT) is a biomarker for poor prognosis and allows tumorigenesis and invasion in colon cancer. causal interaction,diagnostic usage,unassigned 4,1,0 2.4.1.94 Colorectal Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26252736&form=6&db=m Alteration of O-GlcNAcylation affects serine phosphorylation and regulates gene expression and activity of pyruvate kinase M2 in colorectal cancer cells. diagnostic usage,ongoing research,unassigned 1,3,0 2.4.1.94 Diabetes Complications http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29720943&form=6&db=m MicroRNA-200a/200b Modulate High Glucose-Induced Endothelial Inflammation by Targeting O-linked N-Acetylglucosamine Transferase Expression. causal interaction,unassigned 3,0 2.4.1.94 Diabetes Complications http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33192537&form=6&db=m Non-canonical Interaction Between O-Linked N-Acetylglucosamine Transferase and miR-146a-5p Aggravates High Glucose-Induced Endothelial Inflammation. causal interaction,unassigned 2,0 2.4.1.94 Diabetes Mellitus, Type 2 http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9028721&form=6&db=m UDP-N-acetylglucosamine transferase and glutamine: fructose 6-phosphate amidotransferase activities in insulin-sensitive tissues. causal interaction,diagnostic usage,ongoing research,unassigned 2,3,4,0 2.4.1.94 Diabetes Mellitus, Type 2 http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22314054&form=6&db=m O-GlcNAcase is essential for embryonic development and maintenance of genomic stability. unassigned - 2.4.1.94 Diabetic Cardiomyopathies http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17135297&form=6&db=m Impact of Type 2 diabetes and aging on cardiomyocyte function and O-linked N-acetylglucosamine levels in the heart. unassigned - 2.4.1.94 Familial Primary Pulmonary Hypertension http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25663381&form=6&db=m O-GlcNAc Transferase Directs Cell Proliferation in Idiopathic Pulmonary Arterial Hypertension. causal interaction,ongoing research,unassigned 2,1,0 2.4.1.94 Familial Primary Pulmonary Hypertension http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31847126&form=6&db=m O-GlcNAc Transferase Regulates Angiogenesis in Idiopathic Pulmonary Arterial Hypertension. causal interaction,unassigned 4,0 2.4.1.94 Heart Failure http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25495821&form=6&db=m The role of O-GlcNAc transferase in regulating the gene transcription of developing and failing hearts. causal interaction,unassigned 3,0 2.4.1.94 Hyperglycemia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11339805&form=6&db=m Hyperglycemia and the O-GlcNAc transferase in rat aortic smooth muscle cells: elevated expression and altered patterns of O-GlcNAcylation. causal interaction,diagnostic usage,ongoing research,unassigned 1,3,4,0 2.4.1.94 Hyperlipidemias http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32375037&form=6&db=m Islet O-GlcNAcylation Is Required for Lipid Potentiation of Insulin Secretion through SERCA2. ongoing research,therapeutic application,unassigned 1,1,0 2.4.1.94 Hypertension http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22128088&form=6&db=m Cardiac O-GlcNAc signaling is increased in hypertrophy and heart failure. ongoing research,unassigned 2,0 2.4.1.94 Hypertension http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25663381&form=6&db=m O-GlcNAc Transferase Directs Cell Proliferation in Idiopathic Pulmonary Arterial Hypertension. causal interaction,ongoing research,unassigned 2,1,0 2.4.1.94 Hypertension http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31847126&form=6&db=m O-GlcNAc Transferase Regulates Angiogenesis in Idiopathic Pulmonary Arterial Hypertension. causal interaction,unassigned 4,0 2.4.1.94 Influenza, Human http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32494619&form=6&db=m O-GlcNAc transferase promotes influenza A virus-induced cytokine storm by targeting interferon regulatory factor-5. unassigned - 2.4.1.94 Insulin Resistance http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12136128&form=6&db=m Altered glycan-dependent signaling induces insulin resistance and hyperleptinemia. causal interaction,therapeutic application,unassigned 3,1,0 2.4.1.94 Insulin Resistance http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18288188&form=6&db=m Phosphoinositide signalling links O-GlcNAc transferase to insulin resistance. unassigned - 2.4.1.94 Insulin Resistance http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29525407&form=6&db=m Skeletal muscle O-GlcNAc transferase is important for muscle energy homeostasis and whole-body insulin sensitivity. causal interaction,therapeutic application,unassigned 4,2,0 2.4.1.94 Insulin Resistance http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29944994&form=6&db=m Neuronal O-GlcNAc transferase regulates appetite, body weight, and peripheral insulin resistance. therapeutic application,unassigned 2,0 2.4.1.94 Insulin Resistance http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32601203&form=6&db=m OGT suppresses S6K1-mediated macrophage inflammation and metabolic disturbance. ongoing research,unassigned 2,0 2.4.1.94 Intellectual Disability http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28302723&form=6&db=m Identification and Characterization of a Missense Mutation in the O-GlcNAc Transferase Gene that Segregates with X-Linked Intellectual Disability. causal interaction,unassigned 1,0 2.4.1.94 Intellectual Disability http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29606577&form=6&db=m The O-GlcNAc Transferase Intellectual Disability Mutation L254F Distorts the TPR Helix. unassigned - 2.4.1.94 Intellectual Disability http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29769320&form=6&db=m O-GlcNAc transferase missense mutations linked to X-linked intellectual disability deregulate genes involved in cell fate determination and signaling. causal interaction,unassigned 2,0 2.4.1.94 Intellectual Disability http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31296563&form=6&db=m Catalytic deficiency of O-GlcNAc transferase leads to X-linked intellectual disability. causal interaction,unassigned 4,0 2.4.1.94 Intellectual Disability http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31627256&form=6&db=m A missense mutation in the catalytic domain of O-GlcNAc transferase links perturbations in protein O-GlcNAcylation to X-linked intellectual disability. causal interaction,unassigned 2,0 2.4.1.94 Intellectual Disability http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32080367&form=6&db=m An intellectual disability syndrome with single-nucleotide variants in O-GlcNAc transferase. unassigned - 2.4.1.94 Intellectual Disability http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33356293&form=6&db=m Generation of an Interactome for the Tetratricopeptide Repeat Domain of O-GlcNAc Transferase Indicates a Role for the Enzyme in Intellectual Disability. unassigned - 2.4.1.94 Leukemia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26678539&form=6&db=m Mixed Lineage Leukemia 5 (MLL5) Protein Stability Is Cooperatively Regulated by O-GlcNac Transferase (OGT) and Ubiquitin Specific Protease 7 (USP7). therapeutic application,unassigned 1,0 2.4.1.94 Liver Cirrhosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31672932&form=6&db=m O-GlcNAc transferase suppresses necroptosis and liver fibrosis. ongoing research,therapeutic application,unassigned 1,1,0 2.4.1.94 Liver Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28347804&form=6&db=m O-GlcNAc transferase promotes fatty liver-associated liver cancer through inducing palmitic acid and activating endoplasmic reticulum stress. unassigned - 2.4.1.94 Liver Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33909326&form=6&db=m The crosstalk network of XIST/miR-424-5p/OGT mediates RAF1 glycosylation and participates in the progression of liver cancer. ongoing research,unassigned 3,0 2.4.1.94 Liver Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34046694&form=6&db=m Dual regulation of fatty acid synthase (FASN) expression by O-GlcNAc transferase (OGT) and mTOR pathway in proliferating liver cancer cells. causal interaction,ongoing research,unassigned 1,2,0 2.4.1.94 Lung Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25773598&form=6&db=m Histone demethylase LSD2 acts as an E3 ubiquitin ligase and inhibits cancer cell growth through promoting proteasomal degradation of OGT. ongoing research,therapeutic application,unassigned 1,1,0 2.4.1.94 Lymphatic Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26374642&form=6&db=m Proteomic analysis of O-GlcNAcylated proteins in invasive ductal breast carcinomas with and without lymph node metastasis. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,3,2,1 2.4.1.94 Melanoma, Experimental http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28536142&form=6&db=m Augmented TME O-GlcNAcylation Promotes Tumor Proliferation through the Inhibition of p38 MAPK. causal interaction,ongoing research,therapeutic application,unassigned 4,3,1,0 2.4.1.94 Myocardial Infarction http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22128088&form=6&db=m Cardiac O-GlcNAc signaling is increased in hypertrophy and heart failure. ongoing research,unassigned 2,0 2.4.1.94 Neoplasm Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22275356&form=6&db=m Critical role of O-GlcNAc transferase in prostate cancer invasion, angiogenesis and metastasis. causal interaction,diagnostic usage,ongoing research,unassigned 3,4,3,0 2.4.1.94 Neoplasm Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24214978&form=6&db=m O-GlcNAcylation of cofilin promotes breast cancer cell invasion. causal interaction,unassigned 4,0 2.4.1.94 Neoplasm Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26374642&form=6&db=m Proteomic analysis of O-GlcNAcylated proteins in invasive ductal breast carcinomas with and without lymph node metastasis. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,3,2,1 2.4.1.94 Neoplasm Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28499244&form=6&db=m MicroRNA-24-1 suppresses mouse hepatoma cell invasion and metastasis via directly targeting O-GlcNAc transferase. causal interaction,diagnostic usage,unassigned 1,1,0 2.4.1.94 Neoplasm Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31933944&form=6&db=m Increased expression of O-GlcNAc transferase (OGT) is a biomarker for poor prognosis and allows tumorigenesis and invasion in colon cancer. causal interaction,diagnostic usage,unassigned 4,1,0 2.4.1.94 Neoplasm Metastasis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33307156&form=6&db=m Exosomal O-GlcNAc transferase from esophageal carcinoma stem cell promotes cancer immunosuppression through up-regulation of PD-1 in CD8+ T cells. ongoing research,unassigned 2,0 2.4.1.94 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21519190&form=6&db=m O-GlcNAc transferase: a sweet new cancer target. therapeutic application,unassigned 2,0 2.4.1.94 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22314054&form=6&db=m O-GlcNAcase is essential for embryonic development and maintenance of genomic stability. unassigned - 2.4.1.94 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24857547&form=6&db=m O-GlcNAcylation regulates cancer metabolism and survival stress signaling via regulation of the HIF-1 pathway. unassigned - 2.4.1.94 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25000257&form=6&db=m OGA heterozygosity suppresses intestinal tumorigenesis in Apc(min/+) mice. ongoing research,unassigned 1,0 2.4.1.94 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25636967&form=6&db=m mTOR/MYC Axis Regulates O-GlcNAc Transferase (OGT) Expression and O-GlcNAcylation in Breast Cancer. ongoing research,unassigned 2,0 2.4.1.94 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26318312&form=6&db=m MAPK/ERK signaling pathway-induced hyper-O-GlcNAcylation enhances cancer malignancy. causal interaction,therapeutic application,unassigned 3,1,0 2.4.1.94 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26835421&form=6&db=m O-GlcNAcylation and the Metabolic Shift in High-Proliferating Cells: All the Evidence Suggests that Sugars Dictate the Flux of Lipid Biogenesis in Tumor Processes. diagnostic usage,unassigned 1,0 2.4.1.94 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27252680&form=6&db=m Silencing the Nucleocytoplasmic O-GlcNAc Transferase Reduces Proliferation, Adhesion, and Migration of Cancer and Fetal Human Colon Cell Lines. ongoing research,unassigned 4,0 2.4.1.94 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27716624&form=6&db=m Targeting the hexosamine biosynthetic pathway and O-linked N-acetylglucosamine cycling for therapeutic and imaging capabilities in diffuse large B-cell lymphoma. ongoing research,unassigned 1,0 2.4.1.94 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28536142&form=6&db=m Augmented TME O-GlcNAcylation Promotes Tumor Proliferation through the Inhibition of p38 MAPK. causal interaction,ongoing research,therapeutic application,unassigned 4,3,1,0 2.4.1.94 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28628081&form=6&db=m O-GlcNAcylation of fumarase maintains tumour growth under glucose deficiency. causal interaction,unassigned 4,0 2.4.1.94 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28670495&form=6&db=m Bitterness in sugar: O-GlcNAcylation aggravates pre-B acute lymphocytic leukemia through glycolysis via the PI3K/Akt/c-Myc pathway. unassigned - 2.4.1.94 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29059153&form=6&db=m Nutrient sensor O-GlcNAc transferase controls cancer lipid metabolism via SREBP-1 regulation. causal interaction,therapeutic application,unassigned 3,1,0 2.4.1.94 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29115822&form=6&db=m Single Quantum Dot-Based Nanosensor for Sensitive Detection of O-GlcNAc Transferase Activity. causal interaction,unassigned 1,0 2.4.1.94 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30052810&form=6&db=m Proteomic analysis of the OGT interactome: novel links to epithelial-mesenchymal transition and metastasis of cervical cancer. causal interaction,unassigned 2,0 2.4.1.94 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30237786&form=6&db=m Real Talk: The Inter-play Between the mTOR, AMPK, and Hexosamine Biosynthetic Pathways in Cell Signaling. causal interaction,unassigned 3,0 2.4.1.94 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30853938&form=6&db=m Cyclin D1 Stability Is Partly Controlled by O-GlcNAcylation. ongoing research,unassigned 3,0 2.4.1.94 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30987996&form=6&db=m DR4-Ser424 O-GlcNAcylation Promotes Sensitization of TRAIL-Tolerant Persisters and TRAIL-Resistant Cancer Cells to Death. causal interaction,ongoing research,therapeutic application,unassigned 1,4,1,0 2.4.1.94 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31281487&form=6&db=m O-GlcNAc modification of Sox2 regulates self-renewal in pancreatic cancer by promoting its stability. diagnostic usage,ongoing research,unassigned 1,3,0 2.4.1.94 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31933944&form=6&db=m Increased expression of O-GlcNAc transferase (OGT) is a biomarker for poor prognosis and allows tumorigenesis and invasion in colon cancer. causal interaction,diagnostic usage,unassigned 4,1,0 2.4.1.94 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31974291&form=6&db=m O-GlcNAc Transferase Regulates Cancer Stem-like Potential of Breast Cancer Cells. causal interaction,diagnostic usage,ongoing research,therapeutic application 2,1,1,2 2.4.1.94 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32611550&form=6&db=m Inhibition of O-GlcNAc Transferase Renders Prostate Cancer Cells Dependent on CDK9. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,2,3,1 2.4.1.94 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32994395&form=6&db=m Mutual regulation between OGT and XIAP to control colon cancer cell growth and invasion. causal interaction,unassigned 3,0 2.4.1.94 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33251387&form=6&db=m MicroRNA-7-5p's role in the O-GlcNAcylation and cancer metabolism. causal interaction,ongoing research,unassigned 3,3,0 2.4.1.94 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33307156&form=6&db=m Exosomal O-GlcNAc transferase from esophageal carcinoma stem cell promotes cancer immunosuppression through up-regulation of PD-1 in CD8+ T cells. ongoing research,unassigned 2,0 2.4.1.94 Nervous System Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15892570&form=6&db=m Does O-GlcNAc play a role in neurodegenerative diseases? unassigned - 2.4.1.94 Neurodegenerative Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16051707&form=6&db=m A Caenorhabditis elegans model of insulin resistance: altered macronutrient storage and dauer formation in an OGT-1 knockout. causal interaction,unassigned 2,0 2.4.1.94 Neurodegenerative Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22988095&form=6&db=m O-GlcNAc cycling mutants modulate proteotoxicity in Caenorhabditis elegans models of human neurodegenerative diseases. causal interaction,unassigned 4,0 2.4.1.94 Neurodegenerative Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29115822&form=6&db=m Single Quantum Dot-Based Nanosensor for Sensitive Detection of O-GlcNAc Transferase Activity. causal interaction,unassigned 1,0 2.4.1.94 Obesity http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30237786&form=6&db=m Real Talk: The Inter-play Between the mTOR, AMPK, and Hexosamine Biosynthetic Pathways in Cell Signaling. causal interaction,unassigned 3,0 2.4.1.94 Obesity http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31924761&form=6&db=m O-GlcNAc transferase inhibits visceral fat lipolysis and promotes diet-induced obesity. causal interaction,unassigned 2,0 2.4.1.94 Osteosarcoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32266091&form=6&db=m ROCK2 mediates osteosarcoma progression and TRAIL resistance by modulating O-GlcNAc transferase degradation. causal interaction,therapeutic application,unassigned 3,2,0 2.4.1.94 Ovarian Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30555541&form=6&db=m Down-regulation of OGT promotes cisplatin resistance by inducing autophagy in ovarian cancer. causal interaction,unassigned 1,0 2.4.1.94 Placental Insufficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34203166&form=6&db=m Disruption of O-Linked N-Acetylglucosamine Signaling in Placenta Induces Insulin Sensitivity in Female Offspring. causal interaction,unassigned 2,0 2.4.1.94 Prostatic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22275356&form=6&db=m Critical role of O-GlcNAc transferase in prostate cancer invasion, angiogenesis and metastasis. causal interaction,diagnostic usage,ongoing research,unassigned 3,4,3,0 2.4.1.94 Prostatic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23720054&form=6&db=m O-GlcNAc Transferase Integrates Metabolic Pathways to Regulate the Stability of c-MYC in Human Prostate Cancer Cells. diagnostic usage,ongoing research,unassigned 1,3,0 2.4.1.94 Prostatic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26824323&form=6&db=m Inhibition of O-GlcNAc transferase activity reprograms prostate cancer cell metabolism. diagnostic usage,therapeutic application,unassigned 1,1,0 2.4.1.94 Prostatic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31149037&form=6&db=m High OGT activity is essential for MYC-driven proliferation of prostate cancer cells. causal interaction,diagnostic usage,unassigned 3,3,0 2.4.1.94 Prostatic Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32611550&form=6&db=m Inhibition of O-GlcNAc Transferase Renders Prostate Cancer Cells Dependent on CDK9. causal interaction,diagnostic usage,ongoing research,therapeutic application 3,2,3,1 2.4.1.94 protein n-acetylglucosaminyltransferase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31131693&form=6&db=m O-GlcNAc Transferase Promotes Compensated Cardiac Function and Protein Kinase A O-GlcNAcylation During Early and Established Pathological Hypertrophy From Pressure Overload. causal interaction,unassigned 2,0 2.4.1.94 Proteinuria http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29954945&form=6&db=m O-GlcNAcylation reduces proximal tubule protein reabsorption and promotes proteinuria in spontaneously hypertensive rats. ongoing research,unassigned 2,0 2.4.1.94 Sarcoma, Ewing http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27070276&form=6&db=m Reduced O-GlcNAcase expression promotes mitotic errors and spindle defects. unassigned - 2.4.1.94 Starvation http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25840568&form=6&db=m O-GlcNAc modification is essential for the regulation of autophagy in Drosophila melanogaster. causal interaction,unassigned 3,0 2.4.1.94 Urinary Bladder Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32174982&form=6&db=m Blockage of O-linked GlcNAcylation induces AMPK-dependent autophagy in bladder cancer cells. unassigned - 2.4.1.94 Urinary Bladder Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33488099&form=6&db=m O-GlcNAcylation Enhances NUSAP1 Stability and Promotes Bladder Cancer Aggressiveness. diagnostic usage,unassigned 1,0 2.4.1.94 Uterine Cervical Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27482104&form=6&db=m O-linked GlcNAcylation elevated by HPV E6 mediates viral oncogenesis. ongoing research,therapeutic application,unassigned 4,1,0 2.4.1.94 Uterine Cervical Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31489252&form=6&db=m Metformin inhibits cervical cancer cell proliferation via decreased AMPK O-GlcNAcylation. therapeutic application,unassigned 1,0 2.4.1.94 Virus Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16014901&form=6&db=m Identification of secret agent as the O-GlcNAc transferase that participates in Plum pox virus infection. therapeutic application,unassigned 1,0 2.4.1.94 Walker-Warburg Syndrome http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24041696&form=6&db=m GTDC2 modifies O-mannosylated ?-dystroglycan in the endoplasmic reticulum to generate N-acetyl glucosamine epitopes reactive with CTD110.6 antibody. ongoing research,unassigned 2,0