Cloned (Comment) | Organism |
---|---|
Huh7 and HepG2 cells are transiently transfected by both Mgat5 expression vector plasmid and empty vector plasmid as a control | Homo sapiens |
Protein Variants | Comment | Organism |
---|---|---|
L188R | site-directed mutagenesis, inactive mutant | Homo sapiens |
additional information | generation of a stable BEL7404 Tet-on-Mgat5 cell line in which human Mgat5 can be specifically induced by doxycycline to explore functional alterations after Mgat5 overexpression | Homo sapiens |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Homo sapiens | Q09328 | gene MGAT5 | - |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
Hep-G2 cell | the cells show lower enzyme activity | Homo sapiens | - |
hepatocellular carcinoma cell | - |
Homo sapiens | - |
Huh-7 cell | the cells show lower enzyme activity | Homo sapiens | - |
Synonyms | Comment | Organism |
---|---|---|
Mgat5 | - |
Homo sapiens |
N-acetylglucosaminyltransferase V | - |
Homo sapiens |
General Information | Comment | Organism |
---|---|---|
malfunction | Mgat5 overexpression increases p21-activated kinase 1 (PAK1) expression and upregulated beta-1-6-GlcNAc branched N-glycosylation. Mgat5 overexpression promotes anchorage-independent growth and inhibits anoikis in hepatoma cells. shRNA-mediated PAK1 knockdown and kinase inactivation with kinase dead mutant PAK1 K299R coexpression or allosteric inhibitor P21-activated kinase inhibitor III (IPA3) treatment reverses anoikis resistance in Mgat5-overexpressed hepatoma cells. Knockdown of Mgat5 reduces EGFR/PAK1-dependent anoikis resistance, which can be reversed by PAK1 T423E | Homo sapiens |
physiological function | elevated expression and activity of N-acetylglucosaminyltransferase V in hepatocellular carcinoma is a common early event involved in tumor invasion during hepatocarcinogenesis. EGFR/PAK1 signaling dominates Mgat5-induced resistance of hepatoma cells to anoikis | Homo sapiens |