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dc.contributor.authorLópez-Saavedra, Ana-
dc.contributor.authorGómez-Cabello, Daniel-
dc.contributor.authorDomínguez-Sánchez, María S.-
dc.contributor.authorMejías-Navarro, Fernando-
dc.contributor.authorFernández-Ávila, María Jesús-
dc.contributor.authorDinant, Christoffel-
dc.contributor.authorMartínez-Macías, María Isabel-
dc.contributor.authorBartek, Jiri-
dc.contributor.authorHuertas Sánchez, Pablo-
dc.date.accessioned2018-05-25T12:36:35Z-
dc.date.available2018-05-25T12:36:35Z-
dc.date.issued2016-
dc.identifierdoi: 10.1038/ncomms12364-
dc.identifiere-issn: 2041-1723-
dc.identifier.citationNature Communications 7: 12364 (2016)-
dc.identifier.urihttp://hdl.handle.net/10261/165148-
dc.description.abstractThere are two major and alternative pathways to repair DNA double-strand breaks: non-homologous end-joining and homologous recombination. Here we identify and characterize novel factors involved in choosing between these pathways; in this study we took advantage of the SeeSaw Reporter, in which the repair of double-strand breaks by homology-independent or -dependent mechanisms is distinguished by the accumulation of green or red fluorescence, respectively. Using a genome-wide human esiRNA (endoribonuclease-prepared siRNA) library, we isolate genes that control the recombination/end-joining ratio. Here we report that two distinct sets of genes are involved in the control of the balance between NHEJ and HR: those that are required to facilitate recombination and those that favour NHEJ. This last category includes CCAR2/DBC1, which we show inhibits recombination by limiting the initiation and the extent of DNA end resection, thereby acting as an antagonist of CtIP.-
dc.description.sponsorshipThis work was funded by a R + D + I grant from the Spanish Ministry of Economy and Competitivity (SAF2010-14877) and an ERC Starting Grant (DSBRECA). A.L.-S. is the recipient of a FPI fellowship from the Spanish Ministry of Economy and Competitivity, and F.M.-N. is funded with an FPU fellowship from the Spanish Ministry of Education. M.I.M.-M. was the recipient of a Juan de la Cierva Postdoctoral Grant. M.S.D.-S. received a EMBO short-term fellowship for this project. J.B. and C.D. were supported by grants from the Danish National Research Foundation (CARD; DNRF125), the Danish Council for Independent Research (DFF-1331-00262) and the Novo Nordisk Foundation (NNF16584).-
dc.publisherNature Publishing Group-
dc.relationinfo:eu-repo/grantAgreement/EC/FP7/278867-
dc.relation.isversionofPublisher's version-
dc.rightsopenAccess-
dc.titleA genome-wide screening uncovers the role of CCAR2 as an antagonist of DNA end resection-
dc.typeartículo-
dc.relation.publisherversionhttps://doi.org/10.1038/ncomms12364-
dc.date.updated2018-05-25T12:36:35Z-
dc.description.versionPeer Reviewed-
dc.language.rfc3066eng-
dc.rights.licensehttp://creativecommons.org/licenses/by/4.0/-
dc.contributor.funderNovo Nordisk Foundation-
dc.contributor.funderDanish Council for Independent Research-
dc.contributor.funderEMBO-
dc.contributor.funderMinisterio de Educación, Cultura y Deporte (España)-
dc.contributor.funderMinisterio de Economía y Competitividad (España)-
dc.contributor.funderEuropean Research Council-
dc.relation.csic-
dc.identifier.funderhttp://dx.doi.org/10.13039/501100003043es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100000781es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100003329es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100003176es_ES
dc.identifier.pmid27503537-
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