|
Fibrosis, Liver
|
0.010 |
Biomarker
|
disease |
BEFREE |
Taken together, these findings identify OGT as a key suppressor of hepatocyte necroptosis, and OGT-LKO mice may serve as an effective spontaneous genetic model of liver fibrosis.
|
31672932 |
2019 |
|
Intellectual Disability
|
0.120 |
GeneticVariation
|
group |
BEFREE |
These data suggest a direct link between changes in the O-GlcNAcome and intellectual disability observed in patients carrying OGT mutations.
|
31627256 |
2020 |
|
Adult Liver Carcinoma
|
0.030 |
AlteredExpression
|
disease |
BEFREE |
Finally, we find that GFAT expression and O-GlcNAc levels are increased in a spontaneous mouse model of liver cancer.
|
31625393 |
2019 |
|
Liver and Intrahepatic Biliary Tract Carcinoma
|
0.030 |
AlteredExpression
|
disease |
BEFREE |
Finally, we find that GFAT expression and O-GlcNAc levels are increased in a spontaneous mouse model of liver cancer.
|
31625393 |
2019 |
|
Malignant neoplasm of liver
|
0.030 |
AlteredExpression
|
disease |
BEFREE |
Finally, we find that GFAT expression and O-GlcNAc levels are increased in a spontaneous mouse model of liver cancer.
|
31625393 |
2019 |
|
Carcinogenesis
|
0.030 |
AlteredExpression
|
phenotype |
BEFREE |
The amounts of the intracellular glycosylation, O-GlcNAc modification, are increased in essentially all tumors when compared to healthy tissue, and lowering O-GlcNAcylation levels results in reduced tumorigenesis and increased cancer cell death.
|
31625393 |
2019 |
|
Myoepithelioma
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
Sharing the unusual clinicopathologic features and the novel fusion, these 2 cases probably represent a distinct tumor entity, whose relationship with myoepithelial tumors and tumorigenic mechanisms exerted by the OGT-FOXO3 fusion remain to be studied.
|
31567281 |
2020 |
|
Hyperproinsulinemia
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
We show that although CPE is not directly OGlcNAc modified in islets, overexpression of the suspected OGT target eIF4G1, previously shown to regulate CPE translation in β-cells, increases islet CPE levels, and fully reverses βOGTKO islet-induced hyperproinsulinemia.
|
31300553 |
2019 |
|
Intellectual Disability
|
0.120 |
Biomarker
|
group |
BEFREE |
Catalytic deficiency of O-GlcNAc transferase leads to X-linked intellectual disability.
|
31296563 |
2019 |
|
Hyperactive behavior
|
0.020 |
AlteredExpression
|
phenotype |
BEFREE |
In summary, disruption of O-GlcNAc cycling (i.e., Hyper- or Hypo-O-GlcNAcylation) promoted EMT at both the molecular and cellular levels, but only Hyper-O-GlcNAcylation provoked cellular proliferation/migration, and cytoskeletal reorganization.
|
31080560 |
2019 |
|
Hepatitis C
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
We discovered that these miRNAs regulate O-linked N-acetylglucosamine (O-GlcNAc) transferase (OGT) protein expression and identified OGT and O-GlcNAcylation as regulators of HCV morphogenesis and infectivity.
|
31076402 |
2020 |
|
Tumor Cell Invasion
|
0.020 |
AlteredExpression
|
phenotype |
BEFREE |
Elevation of O-GlcNAc and GFAT expression by nicotine exposure promotes epithelial-mesenchymal transition and invasion in breast cancer cells.
|
31019204 |
2019 |
|
Renal Cell Carcinoma
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
O-GlcNAcylation levels and O-GlcNAc-transferase (OGT) expression in human RCC cell lines and 10 paired clinical tissues were detected by Western blot and Immunohistochemis-try.
|
30962710 |
2019 |
|
Conventional (Clear Cell) Renal Cell Carcinoma
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
O-GlcNAcylation levels and O-GlcNAc-transferase (OGT) expression in human RCC cell lines and 10 paired clinical tissues were detected by Western blot and Immunohistochemis-try.
|
30962710 |
2019 |
|
Liver carcinoma
|
0.040 |
Biomarker
|
disease |
BEFREE |
We found that the level of total O-GlcNAcylation or OGT protein was increased in hepatocellular carcinoma.
|
30677218 |
2019 |
|
Colorectal Carcinoma
|
0.020 |
Biomarker
|
disease |
BEFREE |
This study not only reveals the novel functional of O-GlcNAcylation in regulating DDX5, but also reveals the carcinogenic effect of the OGT-DDX5 axis in colorectal cancer.
|
30484950 |
2019 |
|
Malignant neoplasm of colon and/or rectum
|
0.020 |
Biomarker
|
disease |
BEFREE |
This study not only reveals the novel functional of O-GlcNAcylation in regulating DDX5, but also reveals the carcinogenic effect of the OGT-DDX5 axis in colorectal cancer.
|
30484950 |
2019 |
|
Malignant Neoplasms
|
0.070 |
Biomarker
|
group |
BEFREE |
Dysregulation of the O-GlcNAc pathway has been linked to the etiology of several diseases such as neurodegenerative and cardiovascular diseases, type 2 diabetes and cancer.
|
30412832 |
2019 |
|
Primary malignant neoplasm
|
0.060 |
Biomarker
|
group |
BEFREE |
Dysregulation of the O-GlcNAc pathway has been linked to the etiology of several diseases such as neurodegenerative and cardiovascular diseases, type 2 diabetes and cancer.
|
30412832 |
2019 |
|
Cardiovascular Diseases
|
0.020 |
Biomarker
|
group |
BEFREE |
Dysregulation of the O-GlcNAc pathway has been linked to the etiology of several diseases such as neurodegenerative and cardiovascular diseases, type 2 diabetes and cancer.
|
30412832 |
2019 |
|
Autoimmune Chronic Hepatitis
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
These finding indicate that O-GlcNAc glycosylation plays a critical role in the activation of Notch signaling, which could promote Treg differentiation in the liver to inhibit T cell infiltration and control disease development in autoimmune hepatitis.
|
30356792 |
2018 |
|
Autoimmune hepatitis
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
These finding indicate that O-GlcNAc glycosylation plays a critical role in the activation of Notch signaling, which could promote Treg differentiation in the liver to inhibit T cell infiltration and control disease development in autoimmune hepatitis.
|
30356792 |
2018 |
|
Malignant Neoplasms
|
0.070 |
Biomarker
|
group |
BEFREE |
Disruptions in the cycling of O-GlcNAc mediated by O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA), respectively, is a driving force for aberrant cell signaling in disease pathologies, such as diabetes, obesity, Alzheimer's disease, and cancer.
|
30237786 |
2018 |
|
Primary malignant neoplasm
|
0.060 |
Biomarker
|
group |
BEFREE |
Disruptions in the cycling of O-GlcNAc mediated by O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA), respectively, is a driving force for aberrant cell signaling in disease pathologies, such as diabetes, obesity, Alzheimer's disease, and cancer.
|
30237786 |
2018 |
|
Diabetes
|
0.040 |
Biomarker
|
disease |
BEFREE |
Disruptions in the cycling of O-GlcNAc mediated by O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA), respectively, is a driving force for aberrant cell signaling in disease pathologies, such as diabetes, obesity, Alzheimer's disease, and cancer.
|
30237786 |
2018 |