title: Regulation of AID, the B-cell genome mutator.
abstract: The mechanisms by which B cells somatically engineer their genomes to generate the vast diversity of antibodies required to challenge the nearly infinite number of antigens that immune systems encounter are of tremendous clinical and academic interest. The DNA cytidine deaminase activation-induced deaminase (AID) catalyzes two of these mechanisms: class switch recombination (CSR) and somatic hypermutation (SHM). Recent discoveries indicate a significant promiscuous targeting of this B-cell mutator enzyme genome-wide. Here we discuss the various regulatory elements that control AID activity and prevent AID from inducing genomic instability and thereby initiating oncogenesis.
authors: Department of Microbiology and Immunology, College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA.
authors: Celia
authors: C
authors: Keim
authors: David
authors: D
authors: Kazadi
authors: Gerson
authors: G
authors: Rothschild
authors: Uttiya
authors: U
authors: Basu
mesh_terms: D056704:Adaptive Immunity; D000818:Animals; D001402:B-Lymphocytes / Q000201:enzymology* / Q000276:immunology*; D043171:Chromosomal Instability; D003564:Cytidine Deaminase / Q000378:metabolism*; D004789:Enzyme Activation; D016678:Genome; D006801:Humans; D017578:Immunoglobulin Class Switching; D016296:Mutagenesis; D027041:Somatic Hypermutation, Immunoglobulin; D000098830:AICDA (Activation-Induced Cytidine Deaminase)
chemical_list: D000098830:AICDA (Activation-Induced Cytidine Deaminase); D003564:Cytidine Deaminase