EC Number   |
General Information |
Reference |
|---|
   2.1.1.63 | malfunction |
enzyme deficiency leads to a tremendously enhanced sensitivity toward alkylation-induced colorectal carcinogenesis |
733613 |
| 2.1.1.63 | malfunction |
O6-methylguanine-DNA methyltransferase-deficient mice show a higher colon cancer frequency than the wild type |
719231 |
| 2.1.1.63 | metabolism |
Mgt1 is a physiological substrate of both the Ubr1-dependent N-end rule pathway and the Ufd4-dependent ubiquitin fusion degradation pathway |
-, 706528 |
| 2.1.1.63 | physiological function |
MGMT promoter methylation modulated by p53 status can partially promote p53 mutation occurrence in advanced lung tumors |
703393 |
| 2.1.1.63 | physiological function |
O6-methylguanine reversal by the enzyme is required for protection against alkylation-induced colon carcinogenesis |
719231 |
| 2.1.1.63 | physiological function |
the DNA repair protein has an essential role in maintaining genomic stability by removing 6-O-methylguanine adducts |
758122 |
| 2.1.1.63 | physiological function |
the DNA repair protein O6-alkylguanine-DNA alkyltransferase is a principal mechanism of cellular resistance to the toxic and mutagenic effects of DNA damage produced by certain monofunctional alkylating agents. ATase operates by the transfer of the offending alkyl groups from the O6 position of guanine and the O4 position of thymine in damaged DNA to a cysteine residue at the active site of the protein. This is an irreversible process that results in the stoichiometric inactivation of the protein |
-, 726406 |
| 2.1.1.63 | physiological function |
the enzyme is a negative effector of glioblastoma multiforme invasion. Enzyme expression inversely correlates with angiogenesis and invasion in glioma |
734674 |
| 2.1.1.63 | physiological function |
the suicide DNA repair protein plays role in the protection against the cytotoxic and mutagenic effects of alkylating agents causing colorectal carcinogenesis |
733613 |
