This is an abbreviated version! For detailed information about N-acetyllactosaminide beta-1,6-N-acetylglucosaminyltransferase, go to the full flat file.
homozygous frameshift mutation c.1163_1166delATCA, p.(Asn388Argfs*20) is the cause of congenital cataract in two affected siblings, pleiotropic effect of the mutation causing congenital cataract and adult I blood group phenotype, overview
knockdown of GCNT3 using GCNT3-specific small interfering RNAs: siGCNT3-1 (GCUACUGCGAGCUGUGUAUTT), and siGCNT3-2 (GCUCAGUGCCGUGGAAAUATT). Reduction of the expression of endogenous GCNT3 by siRNA transfection in SGC7901 and BGC823 cells. Epstein-Barr virus (EBV) miRNA miR-BART1-5p specifically targets GCNT3. miR-BART1-5p suppresses GCNT3 expression, cell proliferation, and migration in EBVnGC, and the MiR-BART1-5p inhibitor increases GCNT3 expression, cell proliferation, and migration in transfected GT39 and GT38 cells. NF-kappaB can activate the expression of multiple miR-BARTs, including miR-BART1-5p
CRISPR-mediated knockout of GCNT3 in pancreatic cancer cells. A significant increase in pancreas weight is observed in Kras mice compared with wild-type mice. Only 6% of the pancreata from Kras mice are free from PanIN lesions and PDAC, whereas 100% of pancreata are normal in wild-type mice
CRISPR-mediated knockout of GCNT3 in pancreatic cancer cells. A significant increase in pancreas weight is observed in Kras mice compared with wild-type mice. Only 6% of the pancreata from Kras mice are free from PanIN lesions and PDAC, whereas 100% of pancreata are normal in wild-type mice