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- W2150551502 abstract "DNA double-strand break repair is essential for maintenance of genome stability. Recent work has implicated a host of chromatin regulators in the DNA-damage response, and although several functional roles have been defined, the mechanisms that control their recruitment to DNA lesions remain unclear. Here we find that efficient double-strand break recruitment of the INO80, SWR-C, NuA4, SWI/SNF and RSC enzymes is inhibited by the non-homologous end-joining machinery, and that their recruitment is controlled by early steps of homologous recombination. Strikingly, we find no significant role for H2A.X phosphorylation in the recruitment of chromatin regulators, but rather their recruitment coincides with reduced levels of H2A.X phosphorylation. Our work indicates that cell cycle position has a key role in DNA repair pathway choice and that recruitment of chromatin regulators is tightly coupled to homologous recombination. Chromatin regulators facilitate repair of DNA double-strand breaks in chromosomal DNA. The authors show that the recruitment of such chromatin regulators to DNA lesions is controlled by the choice of DNA repair pathway." @default.
- W2150551502 created "2016-06-24" @default.
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- W2150551502 date "2013-06-28" @default.
- W2150551502 modified "2023-09-30" @default.
- W2150551502 title "DNA repair choice defines a common pathway for recruitment of chromatin regulators" @default.
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- W2150551502 doi "https://doi.org/10.1038/ncomms3084" @default.
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