EC Number   |
General Information |
Reference |
|---|
    2.1.1.20 | malfunction |
Gnmt knockout mice develop fatty livers when they have increased S-adenosyl-L-methionine |
704524 |
| 2.1.1.20 | malfunction |
Gnmt knockout mice develop hepatocellular carcinoma, hemangioma, dysplastic nodules, fatty nodules and lung metastasis, DNA methyltransferase activity is decreased in 11 weeks old Gnmt knockout mice, the MAPK pathway is activated in female Gnmt knockout mice |
704068 |
| 2.1.1.20 | malfunction |
overexpression of GNMT causes activation of mTOR/raptor downstream signaling and delays G2/M cell cycle progression, which altogether results in cellular senescence |
720481 |
| 2.1.1.20 | malfunction |
siRNA mediated GNMT knockdown results in an inhibition of proliferation, and induces G1 arrest and apoptosis in prostate cancer cell lines. Patients with high GNMT cytoplasmic expression showed significantly lower disease-free survival rates than patients with low expression |
720403 |
| 2.1.1.20 | metabolism |
GNMT is involved in both hepatic methyl group and one-carbon metabolism |
704524 |
| 2.1.1.20 | physiological function |
experimental autoimmune encephalomyelitis severity is reduced significantly in Gnmt-/- mice. Gnmt-/- mice have significantly lower levels of mononuclear cell infiltration and demyelination than the wild-type mice. Expression levels of proinflammatory cytokines, including interferon-gamma and interleukin 17A, are much lower in the spinal cord of Gnmt-/- than in that of wild-type mice. Myelin oligodendrocyte glycoprotein-specific T-cell proliferation and induction of T-helper Th1 and Th17 cells are markedly suppressed in myelin oligodendrocyte glycoprotein-induced Gnmt-/- mice. The number of regulatory T cells is significantly increased in these mice |
734702 |
| 2.1.1.20 | physiological function |
GNMT affects transmethylation kinetics and S-adenosylmethionine synthesis, and facilitates the conservation of methyl groups by limiting homocysteine remethylation fluxes. Restoring GNMT assists methylfolate-dependent reactions and ameliorates the consequences of folate depletion. GNMT expression in vivo improves folate retention and bioavailability in the liver. Loss of GNMT impairs nucleotide biosynthesis. Over-expression of GNMT enhances nucleotide biosynthesis and improves DNA integrity by reducing uracil misincorporation in DNA both in vitro and in vivo |
757469 |
| 2.1.1.20 | physiological function |
GNMT is a tumor suppressor for hepatocellular carcinoma cells and it exerts protective effects in hepatocytes via direct interaction with aflatoxin B1, resulting in reduced aflatoxin B1-DNA adducts formation and cell death |
706826 |
| 2.1.1.20 | physiological function |
GNMT plays a major role in maintaining normal S-adenosyl-L-methionine levels |
704524 |
| 2.1.1.20 | physiological function |
GNMT regulates hepatocellular growth in part through interacting with DEPDC6/DEPTOR and modulating mTOR/raptor signaling pathway |
720481 |
