EC Number   |
Protein Variants |
Reference |
|---|
   2.4.1.147 | more |
C3GnT-deficient mice display a discrete, colonspecific reduction in Muc2 protein and increased permeability of the intestinal barrier. These mice are highly susceptible to experimental triggers of colitis and colorectal adenocarcinoma |
688103 |
| 2.4.1.147 | more |
C3GnT-deficient mice on a C57BL/6 background |
-, 736236 |
| 2.4.1.147 | more |
generation of mutant mice lacking both intestinal core 1- and core 3-derived O-glycans (DKO), phenotype, overview. Generation of mutant C3GnT-/- |
759814 |
| 2.4.1.147 | more |
introduction of a codon-optimized human UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 6 (beta3Gn-T6) gene into Saccharomyces cerevisiae yields increases in beta3Gn-T6 activity but does not alter the level of core 3 production. The highest in vitro activity of beta3Gn-T6 is observed at Mn2+ concentrations of 10 mM and above. Supplementation of MnCl2 to the culture medium yields increases of up to 25% in the accumulation of core 3 on the MUC1ap. The yeast invertase from the core 3-producing strain is less extensively N-glycosylated, but it is partially restored by the addition of MnCl2 to the medium. Physiological Mn2+ concentration in Saccharomyces cerevisiae is insufficient to facilitate optimal synthesis of core 3. Mn2+ supplementation leads to upregulation of reaction of glycosylation in the Golgi, resulting in increases of core 3 production. Control of Mn2+ concentration is important for production of specific mammalian-type glycans in Sacchromyces cerevisiae microsomes |
758840 |
