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Generation and repair of AID-initiated DNA lesions in B lymphocytes |
Zhangguo Chen,Jing H. Wang( ) |
| Integrated Department of Immunology, University of Colorado Anschutz Medical Campus and National Jewish Health, Denver, CO 80206, USA |
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Abstract Activation-induced deaminase (AID) initiates the secondary antibody diversification process in B lymphocytes. In mammalian B cells, this process includes somatic hypermutation (SHM) and class switch recombination (CSR), both of which require AID. AID induces U:G mismatch lesions in DNA that are subsequently converted into point mutations or DNA double stranded breaks during SHM/CSR. In a physiological context, AID targets immunoglobulin (Ig) loci to mediate SHM/CSR. However, recent studies reveal genome-wide access of AID to numerous non-Ig loci. Thus, AID poses a threat to the genome of B cells if AID-initiated DNA lesions cannot be properly repaired. In this review, we focus on the molecular mechanisms that regulate the specificity of AID targeting and the repair pathways responsible for processing AID-initiated DNA lesions.
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| Keywords
class switch recombination
somatic hypermutation
activation-induced deaminase
DNA repair
genomic instability
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Corresponding Author(s):
Jing H. Wang
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Just Accepted Date: 01 May 2014
Issue Date: 21 May 2014
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