期刊
CELL CYCLE
卷 10, 期 23, 页码 3999-4008出版社
TAYLOR & FRANCIS INC
DOI: 10.4161/cc.10.23.18385
关键词
DNA repair; interstrand cross-links; SNM1A exonuclease; XPF-ERCC1 endonuclease; MUS81-EME1 endonuclease; metallo-beta-lactamase family; SLX4
类别
资金
- Cancer Research UK
- New Zealand Top Achiever Scholarship
DNA interstrand cross-links (ICLs) pose a significant threat to genomic and cellular integrity by blocking essential cellular processes, including replication and transcription. In mammalian cells, much ICL repair occurs in association with DNA replication during S phase, following the stalling of a replication fork at the block caused by an ICL lesion. Here, we review recent work showing that the XPF-ERCC1 endonuclease and the hSNM1A exonuclease act in the same pathway, together with SLX4, to initiate ICL repair, with the MUS81-EME1 fork incision activity becoming important in the absence of the XPF-SNM1A-SLX4-dependent pathway. Another nuclease, the Fanconi anemia-associated nuclease (FAN1), has recently been implicated in the repair of ICLs, and we discuss the possible ways in which the activities of different nucleases at the ICL-stalled replication fork may be coordinated. In relation to this, we briefly speculate on the possible role of SLX4, which contains XPF and MUS81-interacting domains, in the coordination of ICL repair nucleases.
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