Balancing AID and DNA repair during somatic hypermutation
摘要：
genes in B cells is crucial for antibody affinity maturation. The reaction is initiated by cytosine deamination of loci by activation induced deaminase (AID) and is completed by error-prone DNA repair enzyme processing of AID-generated uracils. The mechanisms that target SHM specifically to loci are poorly understood. Recently, it has been demonstrated that although AID preferentially targets loci, it acts surprisingly widely on non- loci, many of which are protected from mutation accumulation by high-fidelity DNA repair. We propose that breakdown of this high fidelity repair process helps explain oncogene mutations observed in B-cell tumors, and further, that many oncogenes are vulnerable to AID-mediated DNA breaks and translocations in normal activated B cells.
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关键词：
Animals Humans B-Lymphocytes Cell Transformation, Neoplastic Cytidine Deaminase DNA Substrate Specificity Mutation Oncogenes Antibody Diversity
DOI：
10.1016/j.it.2009.01.007
被引量：
年份：
2009
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