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 (1). It is necessary for somatic hypermutation and class switch recombination in B cells (2), but inappropriate or dysregulated expression AID is often found in tumors and B cell neoplasms (2,3). Although it is structurally and functionally similar to the APOBEC proteins (reviewed in 4), it appears unlikely that AID deaminates dC to dU residues in HIV cDNA as does APOBEC3G (5).
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