EC Number |
General Information |
Reference |
---|
2.1.1.355 | malfunction |
an enzyme deletion mutant shows significant defects in conidiation, perithecium production and fungal virulence. Enzyme deletion results in increased tolerance to osmotic stresses and upregulated Hog1 phosphorylation |
-, 753592 |
2.1.1.355 | malfunction |
during oxidative stress exposure, enzyme mutants show overactivation of stress response genes, rapid depletion of glycogen, and inability to access lipid energy stores |
755057 |
2.1.1.355 | malfunction |
embryonic stem cells lacking the H3K9 HMTase G9a show a significant reduction in DNA methylation of retrotransposons, major satellite repeats and densely methylated CpG-rich promoters |
703442 |
2.1.1.355 | malfunction |
enzyme depletion results in embryonic lethality with severe differentiation defects in embryonic stem cells. Enzyme depletion inhibits cell proliferation in several cancer cell lines |
753662 |
2.1.1.355 | malfunction |
enzyme inhibition attenuates oncogenicity and activates the hypoxia signaling pathway |
755156 |
2.1.1.355 | malfunction |
enzyme inhibition attenuates the proliferation of HMEC-1 cells, nuclear localization of phosphorylated checkpoint kinase 1, and induces cell cycle arrest in G1 phase |
755002 |
2.1.1.355 | malfunction |
enzyme knockdown stimulates myoblast differentiation |
753905 |
2.1.1.355 | malfunction |
enzyme loss blocks germ cell differentiation |
754853 |
2.1.1.355 | malfunction |
G9a deficiency causes loss of imprinting in the placenta but not the embryo |
705682 |
2.1.1.355 | malfunction |
in cultured hepatic cells, enzyme knockdown results in downregulation of insulin receptor, p-AKT and p-GSK3beta |
752821 |