作者: Robert W. Maul , Patricia J. Gearhart
DOI: 10.1016/S0065-2776(10)05006-6
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摘要: In response to an assault by foreign organisms, peripheral B cells can change their antibody affinity and isotype somatically mutating genomic DNA. The ability of a cell modify its DNA is exceptional in light the potential consequences genetic alterations cause human disease cancer. Thus, as expected, this mechanism diversity tightly regulated coordinated through one protein, activation-induced deaminase (AID). AID produces converting cytosine uracil within immunoglobulin loci. deoxyuracil residue mutagenic when paired with deoxyguanosine, since it mimics thymidine during replication. Additionally, manipulate repair pathways so that deoxyuracils are not faithfully repaired. Therefore, intricate balance exists which at multiple stages promote mutation genes, while retaining integrity rest genome. Here we discuss summarize current understanding how functions somatic hypermutation.