EC Number   |
General Information |
Reference |
|---|
   2.1.1.361 | malfunction |
enzyme deficiency confers an impaired glucose metabolism phenotype and thus inhibits the progression of hepatocellular carcinoma tumors |
753183 |
| 2.1.1.361 | malfunction |
enzyme depletion results in decondensed chromosomes and centrosome amplification |
754080 |
| 2.1.1.361 | malfunction |
enzyme gene disruption results in lethality |
753341 |
| 2.1.1.361 | malfunction |
enzyme inhibition attenuates proliferation and induces apoptosis. Cell migration and invasion are suppressed in enzyme-knockdown cells. Enzyme inhibition arrests the cell cycle in the G1/S phase of papillary thyroid cancer cells. Enzyme inhibition suppresses the expression of SREBP1, SCD, FASN and ACC, key molecules involved in lipid metabolism and decreases the level of malondialdehyde in papillary thyroid cancer cells |
754950 |
| 2.1.1.361 | malfunction |
enzyme knockdown inhibits proliferation, induces apoptosis, suppresses migration and invasion of esophageal squamous cell carcinoma cells |
755441 |
| 2.1.1.361 | malfunction |
enzyme loss triggers cellular senescence |
753196 |
| 2.1.1.361 | malfunction |
expression of an enzyme mutant insensitive to degradation during S phase causes the maintenance of monomethylated histone H4 lysine 20 and repeated DNA replication at origins |
754816 |
| 2.1.1.361 | malfunction |
inappropriate enzyme levels result in profound cell cycle defects including the inability to initiate S phase, the re-replication of DNA and the improper timing of mitotic progression |
753174 |
| 2.1.1.361 | metabolism |
enzyme-mediated methylation of histone H4 lysine 20 maintains silent chromatin, in part, by precluding neighboring acetylation on the histone H4 tail |
754714 |
| 2.1.1.361 | physiological function |
methylation of histone H4 lysine 20 by the enzyme is essential for development and viability in Drosophila |
754714 |
