期刊
MUTATION RESEARCH-REVIEWS IN MUTATION RESEARCH
卷 705, 期 3, 页码 228-238出版社
ELSEVIER
DOI: 10.1016/j.mrrev.2010.07.002
关键词
MutL; MutS; Mismatch repair; Nucleotide excision repair; Base excision repair; Somatic hypermutation; Apoptosis
资金
- Natural Sciences and Engineering Research Council of Canada
In model DNA, A pairs with T, and C with G. However, in vivo, the complementarity of the DNA strands may be disrupted by errors in DNA replication, biochemical modification of bases and recombination. In prokaryotic organisms, mispaired bases are recognized by MutS homologs which, together with MutL homologs, initiate Mismatch repair. These same proteins also participate in base excision repair and nucleotide excision repair. In eukaryotes they regulate not just DNA repair but also meiotic recombination, cell-cycle delay and/or apoptosis in response to DNA damage, and hypermutation in immunoglobulin genes. Significantly, the same DNA mismatches that trigger repair in some circumstances trigger non-repair pathways in others. In this review, we argue that mismatch recognition by the MutS proteins is linked to these disparate biological outcomes through regulated interaction of MutL proteins with a wide variety of effector proteins. (C) 2010 Elsevier B.V. All rights reserved.
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