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Di Virgilio, Michela; Callen, Elsa; Yamane, Arito; Zhang, Wenzhu; Jankovic, Mila; Gitlin, Alexander D.; Feldhahn, Niklas; Resch, Wolfgang; Oliveira, Thiago Y.; Chait, Brian T.; Nussenzweig, André; Casellas, Rafael; Robbiani, Davide F.; Nussenzweig, Michel C.
Science (American Association for the Advancement of Science), 02/2013, Letnik: 339, Številka: 6120Journal Article
DNA double-strand breaks (DSBs) represent a threat to the genome because they can lead to the loss of genetic information and chromosome rearrangements. The DNA repair protein p53 binding protein 1 (53BP1) protects the genome by limiting nucleolytic processing of DSBs by a mechanism that requires its phosphorylation, but whether 53BP1 does so directly is not known. Here, we identify Rap1-interacting factor 1 (Rif1) as an ATM (ataxia-telangiectasia mutated) phosphorylation-dependent interactor of 53BP1 and show that absence of Rif1 results in 5′-3′ DNA-end resection in mice. Consistent with enhanced DNA resection, Rif1 deficiency impairs DNA repair in the G 1 and S phases of the cell cycle, interferes with class switch recombination in B lymphocytes, and leads to accumulation of chromosome DSBs.
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in: SICRIS
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