EC Number   |
General Information |
Reference |
|---|
   3.5.4.38 | malfunction |
deficiency in activation-induced deaminase is responsible for a human immunodeficiency |
719247 |
| 3.5.4.38 | malfunction |
when aberrantly expressed in lung or breast tissue, APOBEC3H can contribute to cancer mutagenesis |
757436 |
| 3.5.4.38 | metabolism |
activation-induced deaminase initiated double-strand breaks and mutations may predispose B cells to carcinogenesis |
719582 |
| 3.5.4.38 | metabolism |
APOBEC3B-catalyzed DNA cytosine deamination causes mutations in cancer |
757151 |
| 3.5.4.38 | metabolism |
the APOBEC3 family has many roles, such as restricting endogenous and exogenous retrovirus replication and retrotransposon insertion events and reducing DNA-induced inflammation |
755694 |
| 3.5.4.38 | metabolism |
the enzyme can contribute to cancer through deamination of cytosine to form promutagenic uracil in genomic DNA |
757841 |
| 3.5.4.38 | metabolism |
the enzyme generates cytidine to deoxyuridine mutations in single-stranded DNA, and is capable of restricting replication of HIV-1 by generating mutations in viral genome |
757774 |
| 3.5.4.38 | physiological function |
activation-induced cytidine deaminase (AID) initiates Ig class switch recombination and somatic hypermutation by producing U:G mismatches in DNA. These mismatches also have the potential to induce DNA damage including double-stranded breaks and chromosome translocations |
720891 |
| 3.5.4.38 | physiological function |
activation-induced cytidine deaminase (AID) initiates immunoglobulin class switch DNA recombination (CSR) and somatic hypermutation deaminating deoxycytidines in switch and V(D)J region DNA,respectively, to generate deoxyuracils. Processing of deoxyuracils by uracil DNA glycosylase yields abasic sites, which are excised by apurinic/apyrimidinic endonucleases, eventually generating double strand DNA breaks, the obligatory intermediates of class switch DNA recombination |
720026 |
| 3.5.4.38 | physiological function |
activation-induced cytidine deaminase (AID) is a mutator enzyme that initiates somatic mutation and class switch recombination in B lymphocytes by introducing uracil:guanine mismatches into DNA. Repair pathways process these mismatches to produce point mutations in the Ig variable region or double-stranded DNA breaks in the switch region DNA. The enzyme can also produce off-target DNA damage, including mutations in oncogenes |
720141 |
