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• W2050987046 abstract "Eukaryotic cells choose the pathway to repair DNA double-strand breaks according to the cell-cycle phase, with homologous recombination preferred during S and G2 phases. Now the direct interaction between CDK2 and the C-terminus of Mre11 is revealed and shown to be important for phosphorylation of CtIP. Homologous recombination facilitates accurate repair of DNA double-strand breaks (DSBs) during the S and G2 phases of the cell cycle by using intact sister chromatids as sequence templates. Homologous recombination capacity is maximized in S and G2 by cyclin-dependent kinase (CDK) phosphorylation of CtIP, which subsequently interacts with BRCA1 and the Mre11–Rad50–NBS1 (MRN) complex. Here we show that, in human and mouse, Mre11 controls these events through a direct interaction with CDK2 that is required for CtIP phosphorylation and BRCA1 interaction in normally dividing cells. CDK2 binds the C terminus of Mre11, which is absent in an inherited allele causing ataxia telangiectasia–like disorder. This newly uncovered role for Mre11 does not require ATM activation or nuclease activities. Therefore, functions of MRN are not restricted to DNA damage responses but include regulating homologous recombination capacity during the normal mammalian cell cycle." @default.
• W2050987046 created "2016-06-24" @default.
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• W2050987046 date "2012-01-08" @default.
• W2050987046 modified "2023-10-10" @default.
• W2050987046 title "Mre11 regulates CtIP-dependent double-strand break repair by interaction with CDK2" @default.
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• W2050987046 doi "https://doi.org/10.1038/nsmb.2212" @default.
• W2050987046 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3272152" @default.
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• W2050987046 hasPublicationYear "2012" @default.
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