Background
Activation-induced cytidine deaminase (AID) was initially discovered as a homolog of the apolipoprotein B RNA-editing cytidine deaminase 1 (APOBEC1) that showed cytidine deaminase properties in stimulated B cell lines. It is necessary for somatic hypermutation and class switch recombination in B cells, but inappropriate or dysregulated expression AID is often found in tumors and B cell neoplasms. Although it is structurally and functionally similar to the APOBEC proteins, it appears unlikely that AID deaminates dC to dU residues in HIV cDNA as does APOBEC3G. |
Reference
1. Muramatsu M, Sankaranand VS, Anant S, et al. Specific expression of activation-induced cytidine deaminase (AID), a novel member of the RNA-editing deaminase family in germinal center B cells. J. Biol. Chem. 1999; 274:18470-6.
2. Muramatsu M, Kinoshita K, Fagarasan S, et al. Class switch recombination and hypermutation require activation-induced cytidine deaminase (AID), a potential RNA editing enzyme. Cell 2000; 102:553-63.
3. Greeve J, Philipsen A, Krause K, et al. Expression of activation-induced cytidine deaminase in human B-cell Hodgkin lymphomas. Blood 2003; 101:3574-80.
4. Cascalho M. Advantages and disadvantages of cytidine deamination. J. Immunol. 2004; 172:6513-8.
5. Sheehy AM, Gaddis NC, Choi JD, et al. Isolation of a human gene that inhibits HIV-1 infection and is suppressed by the viral Vif protein. Nature 2002; 418:646-50.
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