Evidence for base excision repair processing of DNA interstrand crosslinks

被引：19
作者：
Kothandapani, Anbarasi [1 ]
Patrick, Steve M. [1 ]
机构：
[1] Univ Toledo, Dept Biochem & Canc Biol, Toledo, OH 43614 USA
来源：
MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS | 2013年 / 743卷
基金：
美国国家卫生研究院;
关键词：
AP endonuclease; Base excision repair; BCNU; Cisplatin; DNA glycosylase; Interstrand crosslinks; Mitomycin C; Nitrogen mustard; Oxaliplatin; Psoralen; DNA Polymerase beta; APURINIC/APYRIMIDINIC ENDONUCLEASE ACTIVITY; ENHANCES CELLULAR-SENSITIVITY; CANCER-ASSOCIATED VARIANTS; SMALL-MOLECULE INHIBITORS; LONG-PATCH REPAIR; POLYMERASE-BETA; HOMOLOGOUS RECOMBINATION; CISPLATIN CYTOTOXICITY; APHIDICOLIN GLYCINATE; THERAPEUTIC TARGETS;
D O I：
10.1016/j.mrfmmm.2012.11.007
中图分类号：
Q81 [生物工程学（生物技术）]; Q93 [微生物学];
学科分类号：
071005 ; 0836 ; 090102 ; 100705 ;
摘要：
Many bifunctional alkylating agents and anticancer drugs exert their cytotoxicity by producing cross links between the two complementary strands of DNA, termed interstrand crosslinks (ICLs). This blocks the strand separating processes during DNA replication and transcription, which can lead to cell cycle arrest and apoptosis. Cells use multiple DNA repair systems to eliminate the ICLs. Concerted action of repair proteins involved in Nucleotide Excision Repair and Homologous Recombination pathways are suggested to play a key role in the ICL repair. However, recent studies indicate a possible role for Base Excision Repair (BER) in mediating the cytotoxicity of ICL inducing agents in mammalian cells. Elucidating the mechanism of BER mediated modulation of ICL repair would help in understanding the recognition and removal of ICLs and aid in the development of potential therapeutic agents. In this review, the influence of BER proteins on ICL DNA repair and the possible mechanisms of action are discussed. (C) 2012 Elsevier B.V. All rights reserved.
引用
收藏
页码：44 / 52
页数：9
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