EC Number |
General Information |
Reference |
---|
2.4.1.101 | evolution |
sequence alignment reveals that the Trypanosoma brucei enzyme is far removed from the metazoan GnTI family and suggests that the parasite has adapted the beta3-glycosyltransferase family to catalyze beta1-2 linkages. It belongs to a family of putative UDP-sugar-dependent glycosyltransferases with similarity to the mammalian beta1-3-glycosyltransferase family. Enzyme TbGnTI transfers UDP-GlcNAc to biantennary Man3GlcNAc2, but not to triantennary Man5GlcNAc2, which is the preferred substrate for metazoan enzymes |
-, 736466 |
2.4.1.101 | evolution |
the modification in the Golgi of N-glycans by N-acetylglucosaminyltransferase I (GlcNAc-TI, MGAT1) can be considered to be a hallmark of multicellular eukaryotes as it is found in all metazoans and plants, but rarely in unicellular organisms |
758843 |
2.4.1.101 | malfunction |
downregulation of MGAT1 inhibits glioma cell proliferation and migration, overview. Glut1 protein expression is significantly decreased in MGAT1 knockdown cells, but there is no significant change in Glut3. Activation of EGFR signalling by HB-EGF can rescue the inhibitory effects of MGAT1 knockdown on the expression of Glut1, but downregulation of MGAT1 does not significantly change the level of Glut1 mRNA. Downregulation of MGAT1 decreases the complex N-glycan of Glut1. Ectopic expression of Glut1 rescues the inhibitory effects of MGAT1 knockdown on glioma cell proliferation and migration |
759196 |
2.4.1.101 | malfunction |
enzyme-deficient Chlamydomonas reinhardtii cells expressing eukaryotic GnTI from Arabidopsis thaliana exhibit an altered phenotype with large vacuoles, increase of ROS production and accumulation of starch granules, suggesting the activation of stress responses likely due to the perturbation of the Golgi apparatus |
760144 |
2.4.1.101 | malfunction |
enzyme-deficient Chlamydomonas reinhardtii cells expressing eukaryotic GnTI from Phaeodactylum tricornutum exhibit an altered phenotype with large vacuoles, increase of ROS production and accumulation of starch granules, suggesting the activation of stress responses likely due to the perturbation of the Golgi apparatus |
760144 |
2.4.1.101 | malfunction |
Mgat1-null flies are viable but exhibit pronounced defects in locomotion. Neuron-specific RNAi knockdown of Mgat1 in wild-type flies results in locomotory defects, reduced life span, and about 50% reduction in enzyme activity |
723774 |
2.4.1.101 | malfunction |
Mgat1-null mouse embryos die at 9.5-10.5 days after fertilization |
723774 |
2.4.1.101 | malfunction |
modulating N-acetylglucosaminyltransferase I activity in cells can influence antibody effector functions |
721884 |
2.4.1.101 | malfunction |
the bloodstream-form TbGT11 null mutant exhibits significantly modified protein N-glycans but normal growth in vitro and infectivity to rodents |
-, 736466 |
2.4.1.101 | malfunction |
worms with either deletion or RNA-mediated down-regulation of the gly-14 gene are completely resistant to killing by bacteria on PGS medium |
723774 |