Disease on EC 2.4.1.94 - protein N-acetylglucosaminyltransferase
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Alzheimer Disease
O-GlcNAcase is essential for embryonic development and maintenance of genomic stability.
Alzheimer Disease
PET ligands [18F]LSN3316612 and [11C]LSN3316612 quantify O-linked-?-N-acetyl-glucosamine hydrolase in the brain.
Alzheimer Disease
Real Talk: The Inter-play Between the mTOR, AMPK, and Hexosamine Biosynthetic Pathways in Cell Signaling.
Alzheimer Disease
[Effects of Xixin decoction on enzymes related to O-GlcNAc glycosylation of tau proteins in the brain of rats with sporadic Alzheimer's disease].
Aortic Valve Stenosis
Cardiac O-GlcNAc signaling is increased in hypertrophy and heart failure.
Breast Neoplasms
Inhibition of O-GlcNAc transferase activates tumor-suppressor gene expression in tamoxifen-resistant breast cancer cells.
Breast Neoplasms
mTOR/MYC Axis Regulates O-GlcNAc Transferase (OGT) Expression and O-GlcNAcylation in Breast Cancer.
Breast Neoplasms
Nutrient sensor O-GlcNAc transferase regulates breast cancer tumorigenesis through targeting of the oncogenic transcription factor FoxM1.
Breast Neoplasms
O-GlcNAc Transferase Inhibition Differentially Affects Breast Cancer Subtypes.
Breast Neoplasms
O-GlcNAc Transferase Regulates Cancer Stem-like Potential of Breast Cancer Cells.
Breast Neoplasms
Proteomic analysis of O-GlcNAcylated proteins in invasive ductal breast carcinomas with and without lymph node metastasis.
Carcinogenesis
Increased expression of O-GlcNAc transferase (OGT) is a biomarker for poor prognosis and allows tumorigenesis and invasion in colon cancer.
Carcinogenesis
Nutrient sensor O-GlcNAc transferase controls cancer lipid metabolism via SREBP-1 regulation.
Carcinogenesis
Nutrient sensor O-GlcNAc transferase regulates breast cancer tumorigenesis through targeting of the oncogenic transcription factor FoxM1.
Carcinoma
Critical role of O-GlcNAc transferase in prostate cancer invasion, angiogenesis and metastasis.
Carcinoma
Exosomal O-GlcNAc transferase from esophageal carcinoma stem cell promotes cancer immunosuppression through up-regulation of PD-1 in CD8+ T cells.
Carcinoma, Hepatocellular
MicroRNA-24-1 suppresses mouse hepatoma cell invasion and metastasis via directly targeting O-GlcNAc transferase.
Carcinoma, Hepatocellular
O-GlcNAc Transferase Inhibitor Synergistically Enhances Doxorubicin-Induced Apoptosis in HepG2 Cells.
Cardiovascular Diseases
O-GlcNAcase is essential for embryonic development and maintenance of genomic stability.
Cardiovascular Diseases
The role of O-GlcNAc transferase in regulating the gene transcription of developing and failing hearts.
Cholangiocarcinoma
Overexpression of O-GlcNAc-Transferase Associates with Aggressiveness of Mass-Forming Cholangiocarcinoma.
Colonic Neoplasms
Increased expression of O-GlcNAc transferase (OGT) is a biomarker for poor prognosis and allows tumorigenesis and invasion in colon cancer.
Colorectal Neoplasms
Alteration of O-GlcNAcylation affects serine phosphorylation and regulates gene expression and activity of pyruvate kinase M2 in colorectal cancer cells.
Diabetes Complications
MicroRNA-200a/200b Modulate High Glucose-Induced Endothelial Inflammation by Targeting O-linked N-Acetylglucosamine Transferase Expression.
Diabetes Complications
Non-canonical Interaction Between O-Linked N-Acetylglucosamine Transferase and miR-146a-5p Aggravates High Glucose-Induced Endothelial Inflammation.
Diabetes Mellitus, Type 2
O-GlcNAcase is essential for embryonic development and maintenance of genomic stability.
Diabetes Mellitus, Type 2
UDP-N-acetylglucosamine transferase and glutamine: fructose 6-phosphate amidotransferase activities in insulin-sensitive tissues.
Diabetic Cardiomyopathies
Impact of Type 2 diabetes and aging on cardiomyocyte function and O-linked N-acetylglucosamine levels in the heart.
Familial Primary Pulmonary Hypertension
O-GlcNAc Transferase Directs Cell Proliferation in Idiopathic Pulmonary Arterial Hypertension.
Familial Primary Pulmonary Hypertension
O-GlcNAc Transferase Regulates Angiogenesis in Idiopathic Pulmonary Arterial Hypertension.
Heart Failure
The role of O-GlcNAc transferase in regulating the gene transcription of developing and failing hearts.
Hyperglycemia
Hyperglycemia and the O-GlcNAc transferase in rat aortic smooth muscle cells: elevated expression and altered patterns of O-GlcNAcylation.
Hyperlipidemias
Islet O-GlcNAcylation Is Required for Lipid Potentiation of Insulin Secretion through SERCA2.
Hypertension
O-GlcNAc Transferase Directs Cell Proliferation in Idiopathic Pulmonary Arterial Hypertension.
Hypertension
O-GlcNAc Transferase Regulates Angiogenesis in Idiopathic Pulmonary Arterial Hypertension.
Influenza, Human
O-GlcNAc transferase promotes influenza A virus-induced cytokine storm by targeting interferon regulatory factor-5.
Insulin Resistance
Altered glycan-dependent signaling induces insulin resistance and hyperleptinemia.
Insulin Resistance
Neuronal O-GlcNAc transferase regulates appetite, body weight, and peripheral insulin resistance.
Insulin Resistance
OGT suppresses S6K1-mediated macrophage inflammation and metabolic disturbance.
Insulin Resistance
Phosphoinositide signalling links O-GlcNAc transferase to insulin resistance.
Insulin Resistance
Skeletal muscle O-GlcNAc transferase is important for muscle energy homeostasis and whole-body insulin sensitivity.
Intellectual Disability
A missense mutation in the catalytic domain of O-GlcNAc transferase links perturbations in protein O-GlcNAcylation to X-linked intellectual disability.
Intellectual Disability
An intellectual disability syndrome with single-nucleotide variants in O-GlcNAc transferase.
Intellectual Disability
Catalytic deficiency of O-GlcNAc transferase leads to X-linked intellectual disability.
Intellectual Disability
Generation of an Interactome for the Tetratricopeptide Repeat Domain of O-GlcNAc Transferase Indicates a Role for the Enzyme in Intellectual Disability.
Intellectual Disability
Identification and Characterization of a Missense Mutation in the O-GlcNAc Transferase Gene that Segregates with X-Linked Intellectual Disability.
Intellectual Disability
O-GlcNAc transferase missense mutations linked to X-linked intellectual disability deregulate genes involved in cell fate determination and signaling.
Intellectual Disability
The O-GlcNAc Transferase Intellectual Disability Mutation L254F Distorts the TPR Helix.
Leukemia
Mixed Lineage Leukemia 5 (MLL5) Protein Stability Is Cooperatively Regulated by O-GlcNac Transferase (OGT) and Ubiquitin Specific Protease 7 (USP7).
Liver Neoplasms
Dual regulation of fatty acid synthase (FASN) expression by O-GlcNAc transferase (OGT) and mTOR pathway in proliferating liver cancer cells.
Liver Neoplasms
O-GlcNAc transferase promotes fatty liver-associated liver cancer through inducing palmitic acid and activating endoplasmic reticulum stress.
Liver Neoplasms
The crosstalk network of XIST/miR-424-5p/OGT mediates RAF1 glycosylation and participates in the progression of liver cancer.
Lung Neoplasms
Histone demethylase LSD2 acts as an E3 ubiquitin ligase and inhibits cancer cell growth through promoting proteasomal degradation of OGT.
Lymphatic Metastasis
Proteomic analysis of O-GlcNAcylated proteins in invasive ductal breast carcinomas with and without lymph node metastasis.
Melanoma, Experimental
Augmented TME O-GlcNAcylation Promotes Tumor Proliferation through the Inhibition of p38 MAPK.
Myocardial Infarction
Cardiac O-GlcNAc signaling is increased in hypertrophy and heart failure.
Neoplasm Metastasis
Critical role of O-GlcNAc transferase in prostate cancer invasion, angiogenesis and metastasis.
Neoplasm Metastasis
Exosomal O-GlcNAc transferase from esophageal carcinoma stem cell promotes cancer immunosuppression through up-regulation of PD-1 in CD8+ T cells.
Neoplasm Metastasis
Increased expression of O-GlcNAc transferase (OGT) is a biomarker for poor prognosis and allows tumorigenesis and invasion in colon cancer.
Neoplasm Metastasis
MicroRNA-24-1 suppresses mouse hepatoma cell invasion and metastasis via directly targeting O-GlcNAc transferase.
Neoplasm Metastasis
Proteomic analysis of O-GlcNAcylated proteins in invasive ductal breast carcinomas with and without lymph node metastasis.
Neoplasms
Augmented TME O-GlcNAcylation Promotes Tumor Proliferation through the Inhibition of p38 MAPK.
Neoplasms
Bitterness in sugar: O-GlcNAcylation aggravates pre-B acute lymphocytic leukemia through glycolysis via the PI3K/Akt/c-Myc pathway.
Neoplasms
DR4-Ser424 O-GlcNAcylation Promotes Sensitization of TRAIL-Tolerant Persisters and TRAIL-Resistant Cancer Cells to Death.
Neoplasms
Exosomal O-GlcNAc transferase from esophageal carcinoma stem cell promotes cancer immunosuppression through up-regulation of PD-1 in CD8+ T cells.
Neoplasms
Increased expression of O-GlcNAc transferase (OGT) is a biomarker for poor prognosis and allows tumorigenesis and invasion in colon cancer.
Neoplasms
Inhibition of O-GlcNAc Transferase Renders Prostate Cancer Cells Dependent on CDK9.
Neoplasms
MAPK/ERK signaling pathway-induced hyper-O-GlcNAcylation enhances cancer malignancy.
Neoplasms
mTOR/MYC Axis Regulates O-GlcNAc Transferase (OGT) Expression and O-GlcNAcylation in Breast Cancer.
Neoplasms
Mutual regulation between OGT and XIAP to control colon cancer cell growth and invasion.
Neoplasms
Nutrient sensor O-GlcNAc transferase controls cancer lipid metabolism via SREBP-1 regulation.
Neoplasms
O-GlcNAc modification of Sox2 regulates self-renewal in pancreatic cancer by promoting its stability.
Neoplasms
O-GlcNAc Transferase Regulates Cancer Stem-like Potential of Breast Cancer Cells.
Neoplasms
O-GlcNAcase is essential for embryonic development and maintenance of genomic stability.
Neoplasms
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.
Neoplasms
O-GlcNAcylation regulates cancer metabolism and survival stress signaling via regulation of the HIF-1 pathway.
Neoplasms
Proteomic analysis of the OGT interactome: novel links to epithelial-mesenchymal transition and metastasis of cervical cancer.
Neoplasms
Real Talk: The Inter-play Between the mTOR, AMPK, and Hexosamine Biosynthetic Pathways in Cell Signaling.
Neoplasms
Silencing the Nucleocytoplasmic O-GlcNAc Transferase Reduces Proliferation, Adhesion, and Migration of Cancer and Fetal Human Colon Cell Lines.
Neoplasms
Single Quantum Dot-Based Nanosensor for Sensitive Detection of O-GlcNAc Transferase Activity.
Neoplasms
Targeting the hexosamine biosynthetic pathway and O-linked N-acetylglucosamine cycling for therapeutic and imaging capabilities in diffuse large B-cell lymphoma.
Neurodegenerative Diseases
A Caenorhabditis elegans model of insulin resistance: altered macronutrient storage and dauer formation in an OGT-1 knockout.
Neurodegenerative Diseases
O-GlcNAc cycling mutants modulate proteotoxicity in Caenorhabditis elegans models of human neurodegenerative diseases.
Neurodegenerative Diseases
Single Quantum Dot-Based Nanosensor for Sensitive Detection of O-GlcNAc Transferase Activity.
Obesity
O-GlcNAc transferase inhibits visceral fat lipolysis and promotes diet-induced obesity.
Obesity
Real Talk: The Inter-play Between the mTOR, AMPK, and Hexosamine Biosynthetic Pathways in Cell Signaling.
Osteosarcoma
ROCK2 mediates osteosarcoma progression and TRAIL resistance by modulating O-GlcNAc transferase degradation.
Ovarian Neoplasms
Down-regulation of OGT promotes cisplatin resistance by inducing autophagy in ovarian cancer.
Placental Insufficiency
Disruption of O-Linked N-Acetylglucosamine Signaling in Placenta Induces Insulin Sensitivity in Female Offspring.
Prostatic Neoplasms
Critical role of O-GlcNAc transferase in prostate cancer invasion, angiogenesis and metastasis.
Prostatic Neoplasms
High OGT activity is essential for MYC-driven proliferation of prostate cancer cells.
Prostatic Neoplasms
Inhibition of O-GlcNAc transferase activity reprograms prostate cancer cell metabolism.
Prostatic Neoplasms
Inhibition of O-GlcNAc Transferase Renders Prostate Cancer Cells Dependent on CDK9.
Prostatic Neoplasms
O-GlcNAc Transferase Integrates Metabolic Pathways to Regulate the Stability of c-MYC in Human Prostate Cancer Cells.
protein n-acetylglucosaminyltransferase deficiency
O-GlcNAc Transferase Promotes Compensated Cardiac Function and Protein Kinase A O-GlcNAcylation During Early and Established Pathological Hypertrophy From Pressure Overload.
Proteinuria
O-GlcNAcylation reduces proximal tubule protein reabsorption and promotes proteinuria in spontaneously hypertensive rats.
Starvation
O-GlcNAc modification is essential for the regulation of autophagy in Drosophila melanogaster.
Urinary Bladder Neoplasms
Blockage of O-linked GlcNAcylation induces AMPK-dependent autophagy in bladder cancer cells.
Urinary Bladder Neoplasms
O-GlcNAcylation Enhances NUSAP1 Stability and Promotes Bladder Cancer Aggressiveness.
Uterine Cervical Neoplasms
Metformin inhibits cervical cancer cell proliferation via decreased AMPK O-GlcNAcylation.
Uterine Cervical Neoplasms
O-linked GlcNAcylation elevated by HPV E6 mediates viral oncogenesis.
Virus Diseases
Identification of secret agent as the O-GlcNAc transferase that participates in Plum pox virus infection.
Walker-Warburg Syndrome
GTDC2 modifies O-mannosylated ?-dystroglycan in the endoplasmic reticulum to generate N-acetyl glucosamine epitopes reactive with CTD110.6 antibody.
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