EC Number   |
General Information |
Reference |
|---|
   2.4.1.255 | malfunction |
dysregulation of O-GlcNAcylation in response to high glucose or O-GlcNAc transferase expression has been implicated in metabolic diseases and cancer. Knockdown of O-GlcNAc transferase suppresses cell growth and stem-like cell potential of hepatoma cell |
759542 |
| 2.4.1.255 | malfunction |
enzyme knockdown results in nuclear factor-kappaB reporter activation in the cells treated with 10 ng/ml tumor necrosis factor-alpha |
722803 |
| 2.4.1.255 | malfunction |
gain and loss of ogt function produced the same range of defects |
702887 |
| 2.4.1.255 | malfunction |
knockdown of O-GlcNAc transferase and host cell factor C1 decreases gluconeogenesis |
721991 |
| 2.4.1.255 | malfunction |
loss of function of SECRET AGENT, leads to an early flowering phenotype. This results from reduced histone H3 lysine 4 trimethylation (H3K4me3) of FLOWERING LOCUS C (FLC) locus, which encodes a key negative regulator of flowering |
759121 |
| 2.4.1.255 | malfunction |
O-GlcNAc transferase knockout is embryonic lethal in a range of animal models |
758767 |
| 2.4.1.255 | malfunction |
reducing endogenous mOGT expression leads to alterations in mitochondrial structure and function, including Drp1-dependent mitochondrial fragmentation, reduction in mitochondrial membrane potential, and a significant loss of mitochondrial content in the absence of mitochondrial ROS |
759487 |
| 2.4.1.255 | malfunction |
several EOGT mutations that may affect putative N-glycosylation consensus sites are recorded in the cancer database |
759507 |
| 2.4.1.255 | malfunction |
silencing of OGT results in impaired activation of T and B lymphocytes |
703439 |
| 2.4.1.255 | malfunction |
siRNA-mediated knockdown of the enzyme enhances 26S proteasome assembly and activity |
723564 |
