Mutagenic repair of DNA interstrand crosslinks.
Mutagenic repair of DNA interstrand crosslinks.
复制标题
DOI：
10.1002/em.20558
复制
发表时间：
2010-07
影响因子：
2.8
通讯作者：
Li, Lei
中科院分区：
文献类型：
--
作者：
Shen, Xi;Li, Lei
染色体DNA中DNA链间交联（ICLs）的形成会严重阻碍所有必要的DNA功能。近世纪来，双功能烷化剂，也称为DNA交联剂，一直是一类重要的癌症化疗方案。ICL修复的机制在很大程度上仍然难以捉摸。在这里，我们回顾了一个真核细胞诱变ICL修复途径发现的工作从几个实验室。该修复途径，或者称为重组非依赖性ICL修复，涉及核苷酸切除修复（NER）机制和病变旁路聚合酶的切割活性。ICL的修复由双螺旋的一条链上的ICL侧翼的双切口启动;所产生的间隙由病变旁路聚合酶填充。剩余的病变随后通过第二轮NER反应去除。ICL的诱变修复可能与其他细胞机制相互作用，如范可尼贫血途径和ICL的重组修复。这些方面也将讨论。
Formation of DNA interstrand crosslinks (ICLs) in chromosomal DNA imposes acute obstruction of all essential DNA functions. For nearly a century, bifunctional alkylators, also known as DNA crosslinkers, have been an important class of cancer chemotherapeutic regimens. The mechanisms of ICL repair remains largely elusive. Here, we review a eukaryotic mutagenic ICL repair pathway discovered by work from several laboratories. This repair pathway, alternatively termed recombination-independent ICL repair, involves the incision activities of the nucleotide excision repair (NER) mechanism and lesion bypass polymerase(s). Repair of the ICL is initiated by dual incisions flanking the ICL on one strand of the double helix; the resulting gap is filled in by lesion bypass polymerases. The remaining lesion is subsequently removed by a second round of NER reaction. The mutagenic repair of ICL likely interacts with other cellular mechanisms such as the Fanconi anemia pathway and recombinational repair of ICLs. These aspects will also be discussed.
登录
查看更多内容
影响因子：
6.2
作者：
Kahl, Brad S.;Bartlett, Nancy L.;Leonard, John P.;Chen, Ling;Ganjoo, Kristen;Williams, Michael E.;Czuczman, Myron S.;Robinson, K. Sue;Joyce, Robin;van der Jagt, Richard H.;Cheson, Bruce D.
通讯作者：
Cheson, Bruce D.
影响因子：
16
作者：
Ciccia, Alberto;Ling, Chen;West, Stephen C.
通讯作者：
West, Stephen C.
影响因子：
4.3
作者：
McHugh, Peter J.;Sarkar, Sovan
通讯作者：
Sarkar, Sovan
影响因子：
2.9
作者：
Berardini, M;Mackay, W;Loechler, EL
通讯作者：
Loechler, EL
影响因子：
16
作者：
Matsushita, N;Kitao, H;Takata, M
通讯作者：
Takata, M