EC Number   |
General Information |
Reference |
|---|
   2.4.1.150 | malfunction |
analysis of pleiotropic effect of mutations in GCNT2, especially frameshift mutation N388R, causing congenital cataract and a rare adult I blood group phenotype, detailed overview |
759326 |
| 2.4.1.150 | malfunction |
C2GnT2 deficiency, impair of mucosal barrier, increase of susceptibility to colitis, reduced immunoglobulin abundance, loss of all core 4 O-glycan biosynthetic activity |
705696 |
| 2.4.1.150 | malfunction |
ectopic overexpression of GCNT2 enhances cell detachment, adhesion to endothelial cells, cell migration and invasion in vitro, and lung metastasis of breast cancer cells in vivo. Knockdown of GCNT2 expression decreases cell migration and invasion in vitro and lung metastasis in vivo. Diminution of the glycosyltransferase activity of I-branching beta-1,6-N-acetylglucosaminyl transferase 2 (GCNT2) abrogates its cell migration and invasion-promoting function and synergistic effect with TGF-beta to induce EMT, effect of GCNT2 expression knockdown on oncogenic properties, overview |
758992 |
| 2.4.1.150 | malfunction |
GCNT3 overexpression reduces 5-fluorouracil resistance in colorectal cancer (CRC) cells. GCNT3 overexpression reduces proliferation, invasion and changes metabolic capacities of CRC cells. The enzyme's overexpression in epithelial ovarian cancer (EOC) patients is associated with better clinical outcome and response to initial therapy |
760171 |
| 2.4.1.150 | malfunction |
in mouse pancreatic cancer tumors, GCNT3 upregulation is correlated with increased expression of mucins. Aberrant GCNT3 expression is associated with increased mucin production, aggressive tumorigenesis, and reduced survival. CRISPR-mediated knockout of GCNT3 in pancreatic cancer cells reduced proliferation and spheroid formation |
-, 758993 |
| 2.4.1.150 | malfunction |
manipulation of I-branching N-acetylglucosaminyltransferase (GCNT2) expression in esophageal squamous cell carcinoma cells has no effect on cell proliferation. Overexpression of GCNT2 promotes the migration and invasion, and this effect is associated with increased expression of N-cadherin and vimentin and decreased expression of E-cadherin in KYSE30 and EC9706 cells. Knockdown of GCNT2 decreased the expression of N-cadherin and vimentin, increases the expression of E-cadherin, and inhibits the migration and invasion in KYSE150 and EC109 cells |
759012 |
| 2.4.1.150 | malfunction |
miR-BART1-5p directly targets GCNT3. In addition, miR-BART1-5p mimics transfection is observed to reduce cell proliferation and migration, while miR-BART1-5p inhibitor increases cell proliferation and migration following transfection. In conclusion, both miR-BART1-5p and knockdown of GCNT3 inhibit cell proliferation and migration |
760226 |
| 2.4.1.150 | malfunction |
talniflumate alone and in combination with low-dose gefitinib reduces GCNT3 expression, leading to the disrupted production of mucins in vivo and in vitro. Aberrant GCNT3 expression is associated with increased mucin production, aggressive tumorigenesis, and reduced patient survival. CRISPR-mediated knockout of GCNT3 in pancreatic cancer cells reduced proliferation and spheroid formation |
758993 |
| 2.4.1.150 | metabolism |
GCNT2 is a direct target of the TGF-beta-smad pathway and that change in GCNT2 expression modulates EMT induced by TGF-beta1 treatment. Involvement of GCNT2 in EMT and TGF-beta signaling, and further glycosylation modification of E-cadherin by GCNT2, are the underlying integrative mechanisms for breast cancer metastasis. GCNT2 contributes to distal metastasis in vivo |
758992 |
| 2.4.1.150 | metabolism |
integrated transcriptomic and proteomic analyses reveal that GCNT3 is linked to cellular cycle, mitosis and proliferation, response to drugs and metabolism pathways. The vascular epithelial growth factor A (VEGFA) arises as an attractive partner of GCNT3 functions in cell invasion and resistance |
760171 |
