EC Number   |
General Information |
Reference |
|---|
   1.14.11.51 | malfunction |
enzyme deletion accelerates the progressive fertility defect of spr-5 mutant worms |
742235 |
| 1.14.11.51 | malfunction |
enzyme-depleted mesenchymal stem cells exhibit a restricted capacity for bone formation in vivo |
742207 |
| 1.14.11.51 | metabolism |
N6-hydroxymethyladenine exists as an oxidized intermediate during N6-mA demethylation by ALKBH1 |
764442 |
| 1.14.11.51 | physiological function |
Alkbh1 expression in bone marrow mesenchymal stem cells declines during aging. Knockout of Alkbh1 promotes adipogenic differentiation of bone marrow mesenchymal stem cells while inhibits osteogenic differentiation. Bone marrow mesenchymal stem cells -specific Alkbh1 knockout mice exhibit reduced bone mass and increased marrow adiposity. Overexpression of Alkbh1 attenuates bone loss and marrow fat accumulation in aged mice |
764440 |
| 1.14.11.51 | physiological function |
ALKBH1 is critical for the myogenic differentiation of C2C12 cells. Overexpression of ALKBH1 reduces N6-mA levels, enhances proliferation and inhibits differentiation in C2C12 cells. ALKBH1 regulates a subset of genes and impairs multiple signaling required for muscle development |
764640 |
| 1.14.11.51 | physiological function |
ALKBH1 overexpression decreases hepatocellular carcinoma cell viability, induces apoptosis, and decreases migration and invasion |
764811 |
| 1.14.11.51 | physiological function |
enzyme overexpression enhances osteoblastic differentiation of mesenchymal stem cells |
742207 |
| 1.14.11.51 | physiological function |
knockdown of ALKBH1 inhibits adipogenic differentiation in both mesenchymal stem cells and 3T3-L1 preadipocytes, while overexpression of ALKBH1 leads to increased adipogenesis. Hypoxia-inducible factor HIF-1 signaling is a crucial downstream target of ALKBH1 activity. Depletion of ALKBH1 leads to hypermethylation of both HIF-1alpha and its downstream target GYS1 |
765084 |
| 1.14.11.51 | physiological function |
RNAi knockdown of 6mA methyltransferase METTL4 and 6mA demethylase NMAD induce cell cycle arrest at G1 phase and also result in defects of chromosome alignments at metaphase |
764222 |
| 1.14.11.51 | physiological function |
the 6-methyl adenine demethylase activity is very low. The demethylase activity is less than half that of the apurinic/apyrimidinic lyase activity when ALKBH1 samples are assayed using identical buffer conditions. The two enzymatic activities are located in distinct but partially overlapping active sites for the two reactions |
764135 |
