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dc.contributor.authorPrados-Carvajal, Rosario-
dc.contributor.authorLópez-Saavedra, Ana-
dc.contributor.authorCepeda-García, Cristina-
dc.contributor.authorJimeno, Sonia-
dc.contributor.authorHuertas Sánchez, Pablo-
dc.date.accessioned2018-06-06T07:44:00Z-
dc.date.available2018-06-06T07:44:00Z-
dc.date.issued2018-
dc.identifierdoi: 10.1016/j.dnarep.2018.04.003-
dc.identifiere-issn: 1568-7856-
dc.identifierissn: 1568-7864-
dc.identifier.citationDNA Repair 66-67: 11-23 (2018)-
dc.identifier.urihttp://hdl.handle.net/10261/165748-
dc.description.abstractThe appropriate repair of DNA double strand breaks is critical for genome maintenance. Thus, several cellular pathways collaborate to orchestrate a coordinated response. These include the repair of the breaks, which could be achieved by different mechanisms. A key protein involved in the regulation of the repair of broken chromosomes is CtIP. Here, we have found new partners of CtIP involved in the regulation of DNA break repair through affecting DNA end resection. We focus on the splicing complex SF3B and show that its depletion impairs DNA end resection and hampers homologous recombination. Functionally, SF3B controls CtIP function at, as least, two levels: by affecting CtIP mRNA levels and controlling CtIP recruitment to DNA breaks, in a way that requires ATM-mediated phosphorylation of SF3B2 at serine 289. Indeed, overexpression of CtIP rescues the resection defect caused by SF3B downregulation. Strikingly, other SF3B depletion phenotypes, such as impaired homologous recombination or cellular sensitivity to DNA damaging agents, are independent of CtIP levels, suggesting a more general role of SF3B in controlling the response to chromosome breaks.-
dc.description.sponsorshipThis work was funded by a R + D + I grant from the Spanish Ministry of Economy and Competitivity (SAF2013-43255-P) and an ERC Starting Grant (DSBRECA). AL-S is the recipient of a FPI fellowship from the Spanish Ministry of Economy and Competitivity, and RP-C is funded with an FPU fellowship from the Spanish Ministry of Education. CABIMER is supported by the regional government of Andalucia (Junta de Andalucía).-
dc.publisherElsevier-
dc.relationinfo:eu-repo/grantAgreement/MINECO/Plan Estatal de Investigación Científica y Técnica y de Innovación 2013-2016/SAF2013-43255-P-
dc.relationinfo:eu-repo/grantAgreement/EC/FP7/278867-
dc.rightsclosedAccess-
dc.subjectDNA resection-
dc.subjectCtIP-
dc.subjectSF3B-
dc.subjectRNA splicing-
dc.subjectHomologous recombination-
dc.titleMultiple roles of the splicing complex SF3B in DNA end resection and homologous recombination-
dc.typeartículo-
dc.identifier.doi10.1016/j.dnarep.2018.04.003-
dc.date.updated2018-06-06T07:44:00Z-
dc.description.versionPeer Reviewed-
dc.language.rfc3066eng-
dc.contributor.funderJunta de Andalucía-
dc.contributor.funderMinisterio de Economía y Competitividad (España)-
dc.contributor.funderMinisterio de Educación (España)-
dc.contributor.funderEuropean Research Council-
dc.relation.csic-
dc.identifier.funderhttp://dx.doi.org/10.13039/501100003329es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100000781es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100011011es_ES
dc.identifier.pmid29705135-
dc.type.coarhttp://purl.org/coar/resource_type/c_6501es_ES
item.openairetypeartículo-
item.cerifentitytypePublications-
item.grantfulltextnone-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.fulltextNo Fulltext-
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