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• W2003167812 abstract "•SRCAP is a DNA damage response protein•SRCAP promotes DNA-end resection and homologous recombination repair•SRCAP forms a complex with CtIP and is required for CtIP accumulation at DSBs•SRCAP facilitates DNA-end resection by promoting chromatin relaxation BackgroundRepair of DNA double-strand breaks (DSBs) by homologous recombination requires 5′-3′ resection of the DSB ends. In vertebrates, DSB resection is initiated by the collaborative action of CtIP and the MRE11-RAD50-NBS1 (MRN) complex. However, how this process occurs within the context of chromatin is still not well understood.ResultsHere we identify the human SRCAP chromatin remodeling complex as a factor that promotes CtIP-dependent DNA-end resection. We show that SRCAP, which is mutated in Floating-Harbor syndrome, confers resistance to DNA damage-inducing agents and is recruited to DSBs. Moreover, we demonstrate that SRCAP is required for DNA-end resection, and thereby for recruitment of RPA and RAD51 to DSBs, and for the ensuing homologous recombination. Finally, we reveal that SRCAP forms a complex with CtIP and promotes accumulation of CtIP at DSBs through a mechanism involving its ATPase activity.ConclusionsOur study implicates the human SRCAP chromatin remodeling complex as a novel regulator of DNA damage responses that orchestrates proper signaling and repair of DSBs in the context of chromatin. Repair of DNA double-strand breaks (DSBs) by homologous recombination requires 5′-3′ resection of the DSB ends. In vertebrates, DSB resection is initiated by the collaborative action of CtIP and the MRE11-RAD50-NBS1 (MRN) complex. However, how this process occurs within the context of chromatin is still not well understood. Here we identify the human SRCAP chromatin remodeling complex as a factor that promotes CtIP-dependent DNA-end resection. We show that SRCAP, which is mutated in Floating-Harbor syndrome, confers resistance to DNA damage-inducing agents and is recruited to DSBs. Moreover, we demonstrate that SRCAP is required for DNA-end resection, and thereby for recruitment of RPA and RAD51 to DSBs, and for the ensuing homologous recombination. Finally, we reveal that SRCAP forms a complex with CtIP and promotes accumulation of CtIP at DSBs through a mechanism involving its ATPase activity. Our study implicates the human SRCAP chromatin remodeling complex as a novel regulator of DNA damage responses that orchestrates proper signaling and repair of DSBs in the context of chromatin." @default.
• W2003167812 created "2016-06-24" @default.
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• W2003167812 date "2014-09-01" @default.
• W2003167812 modified "2023-10-15" @default.
• W2003167812 title "The Human SRCAP Chromatin Remodeling Complex Promotes DNA-End Resection" @default.
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• W2003167812 doi "https://doi.org/10.1016/j.cub.2014.07.081" @default.
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