Base excision repair: The long and short of it

被引：473
作者：
Robertson A.B. [1 ]
Klungland A. [1 ]
Rognes T. [1 ,2 ]
Leiros I. [3 ]
机构：
[1] Centre for Molecular Biology and Neuroscience, Institute of Medical Microbiology, University of Oslo
[2] Department of Informatics, University of Oslo, 0316 Oslo, Blindern
[3] Norwegian Structural Biology Centre (NorStruct), Department of Chemistry, University of Tromsø
来源：
Cellular and Molecular Life Sciences | 2009年 / 66卷 / 6期
关键词：
Alkylation; Base excision repair; Deamination; DNA damage; Glycosylase; Oxidation;
D O I：
10.1007/s00018-009-8736-z
中图分类号：
学科分类号：
摘要：
Base excision repair (BER) is the primary DNA repair pathway that corrects base lesions that arise due to oxidative, alkylation, deamination, and depurinatiation/depyrimidination damage. BER facilitates the repair of damaged DNA via two general pathways - short-patch and long-patch. The shortpatch BER pathway leads to a repair tract of a single nucleotide. Alternatively, the long-patch BER pathway produces a repair tract of at least two nucleotides. The BER pathway is initiated by one of many DNA glycosylases, which recognize and catalyze the removal of damaged bases. The completion of the BER pathway is accomplished by the coordinated action of at least three additional enzymes. These downstream enzymes carry out strand incision, gap-filling and ligation. The high degree of BER conservation between E. coli and mammals has lead to advances in our understanding of mammalian BER. This review will provide a general overview of the mammalian BER pathway. (Part of a Multi-author Review). © 2009 Birkhäuser Verlag.
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页码：981 / 993
页数：12
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