XRCC1 interactions with base excision repair DNA intermediates

被引:81
|
作者
Nazarkina, Zhanna K.
Khodyreva, Svetlana N.
Marsin, Stephanie
Lavrik, Olga I.
Radicella, J. Pablo
机构
[1] Russian Acad Sci, Siberian Branch, Inst Chem Biol & Fundamental Med, Novosibirsk 630090, Russia
[2] Commissariat Energie Atom, CNRS, CEA, UMR 217,Dept Radiobiol & Radiopathol, F-92265 Fontenay Aux Roses, France
基金
俄罗斯基础研究基金会;
关键词
XRCC1; abasic sites; base excision repair; DNA binding; clustered lesions;
D O I
10.1016/j.dnarep.2006.10.002
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Abasic (AP) sites in DNA arise either spontaneously, or through glycosylase-catalyzed excision of damaged bases. Their removal by the base excision repair (BER) pathway avoids their mutagenic and cytotoxic consequences. XRCC1 coordinates and facilitates single-strand break (SSB) repair and BER in mammalian cells. We report that XRCC1, through its NTD and BRCT1 domains, has affinity for several DNA intermediates in BER. As shown by its capacity to form a covalent complex via Schiffbase, XRCC1 binds AP sites. APE1 suppresses binding of XRCC1 to unincised AP sites however, affinity was higher when the DNA carried an AP-lyase- or APE1-incised AP site. The AP site binding capacity of XRCC1 is enhanced by the presence of strand interruptions in the opposite strand. Binding of XRCC1 to BER DNA intermediates could play an important role to warrant the accurate repair of damaged bases, AP sites or SSBs, in particular in the context of clustered DNA damage. (c) 2006 Elsevier B.V. All rights reserved.
引用
收藏
页码:254 / 264
页数:11
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