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- W2025268178 abstract "The interstrand crosslink (ICL) presents a challenge to both the cell and the scientist. From a clinical standpoint, these lesions are particularly intriguing: ICL-inducing agents are powerful tools in cancer chemotherapy, and spontaneous ICLs have recently been linked with accelerated aging phenotypes. Nevertheless, the ICL repair process has proven difficult to elucidate. Here we discuss recent additions to the current model and argue that the endonuclease xeroderma pigmentosum complementation group F-excision repair cross-complementing rodent repair deficiency complementation group 1 (XPF-ERCC1) has been heretofore misplaced. During nucleotide excision repair, XPF-ERCC1 makes a single-strand nick adjacent to the lesion. XPF-ERCC1 has been thought to play an analogous role in ICL repair. However, recent data has implicated XPF-ERCC1 in homologous recombination. We suggest that this role, rather than its function in nucleotide excision repair, defines its importance to ICL repair." @default.
- W2025268178 created "2016-06-24" @default.
- W2025268178 creator A5020880841 @default.
- W2025268178 creator A5042927941 @default.
- W2025268178 date "2008-02-01" @default.
- W2025268178 modified "2023-09-25" @default.
- W2025268178 title "Interstrand crosslink repair: can XPF-ERCC1 be let off the hook?" @default.
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- W2025268178 doi "https://doi.org/10.1016/j.tig.2007.11.003" @default.
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