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dc.contributor.authorHernández, Gonzaloes_ES
dc.contributor.authorRamírez, María Josées_ES
dc.contributor.authorMinguillón, Jordies_ES
dc.contributor.authorQuiles, Pacoes_ES
dc.contributor.authorRuiz de Garibay, Gorkaes_ES
dc.contributor.authorAza Carmona, Miriames_ES
dc.contributor.authorBogliolo, Massimoes_ES
dc.contributor.authorPujol, Roseres_ES
dc.contributor.authorPrados-Carvajal, Rosarioes_ES
dc.contributor.authorFernández, Juanaes_ES
dc.contributor.authorGarcía, Nadiaes_ES
dc.contributor.authorLópez, Adriàes_ES
dc.contributor.authorGutiérrez-Enríquez, Saraes_ES
dc.contributor.authorDíez, Orlandes_ES
dc.contributor.authorBenitez, Javieres_ES
dc.contributor.authorSalinas, Mónicaes_ES
dc.contributor.authorTeulé, Alexes_ES
dc.contributor.authorBrunet, Joanes_ES
dc.contributor.authorRadice, Paoloes_ES
dc.contributor.authorPeterlongo, Paoloes_ES
dc.contributor.authorSchindler, Detleves_ES
dc.contributor.authorHuertas Sánchez, Pabloes_ES
dc.contributor.authorPuente, Xose S.es_ES
dc.contributor.authorLázaro, Conxies_ES
dc.contributor.authorPujana, Miguel Ángeles_ES
dc.contributor.authorSurrallés, Jordies_ES
dc.date.accessioned2019-04-25T07:06:21Z-
dc.date.available2019-04-25T07:06:21Z-
dc.date.issued2018-03-06-
dc.identifier.citationNature Communications 9: 967 (2018)es_ES
dc.identifier.urihttp://hdl.handle.net/10261/180508-
dc.description.abstractBRCA1 is a tumor suppressor that regulates DNA repair by homologous recombination. Germline mutations in BRCA1 are associated with increased risk of breast and ovarian cancer and BRCA1 deficient tumors are exquisitely sensitive to poly (ADP-ribose) polymerase (PARP) inhibitors. Therefore, uncovering additional components of this DNA repair pathway is of extreme importance for further understanding cancer development and therapeutic vulnerabilities. Here, we identify EDC4, a known component of processing-bodies and regulator of mRNA decapping, as a member of the BRCA1-BRIP1-TOPBP1 complex. EDC4 plays a key role in homologous recombination by stimulating end resection at double-strand breaks. EDC4 deficiency leads to genome instability and hypersensitivity to DNA interstrand crosslinking drugs and PARP inhibitors. Lack-of-function mutations in EDC4 were detected in BRCA1/2-mutation-negative breast cancer cases, suggesting a role in breast cancer susceptibility. Collectively, this study recognizes EDC4 with a dual role in decapping and DNA repair whose inactivation phenocopies BRCA1 deficiencyes_ES
dc.description.sponsorshipSurrallés laboratory is supported by the ICREA-Academia program, the Marató de TV3 (project 464/C/2012), the Spanish Ministry of Health (projects FANCOSTEM and FANCOLEN), the Spanish Ministry of Economy and Competiveness (projects CB06/07/0023, SAF2012-31881, SAF2013-45836-R and SAF2015-64152-R), the European Commission (EUROFANCOLEN project HEALTH-F5-2012-305421 and P-SPHERE COFUND project), the Fanconi Anemia Research Fund Inc., and the “Fondo Europeo de Desarrollo Regional, una manera de hacer Europa” (FEDER). CIBERER is an initiative of the Instituto de Salud Carlos III, Spain. This work was also supported by grants from the Asociación Española Contra el Cáncer (AECC, Hereditary Cancer group, 2010), the Generalitat de Catalunya (SGR 2014-364 and 2014-338), and the Instituto de Salud Carlos III (PIE13/00022-ONCOPROFILE, CP10/00617, PI10/01422, PI12/02585, PI13/00285, PI15/00854, PI16/00563, PI16/01218, and RTICC RD12/0036/0008). S.G.-E. is funded by a Miguel Servet contract from the Instituto de Salud Carlos III.es_ES
dc.language.isoenges_ES
dc.publisherNature Publishing Groupes_ES
dc.relationMINECO/ICTI2013-2016/SAF2012-31881es_ES
dc.relationMINECO/ICTI2013-2016/SAF2013-45836-Res_ES
dc.relationMINECO/ICTI2013-2016/SAF2015-64152-Res_ES
dc.relationinfo:eu-repo/grantAgreement/EC/FP7/305421es_ES
dc.relationinfo:eu-repo/grantAgreement/EC/H2020/665919es_ES
dc.relation.isversionofPublisher's versiones_ES
dc.rightsopenAccesses_ES
dc.titleDecapping protein EDC4 regulates DNA repair and phenocopies BRCA1es_ES
dc.typeartículoes_ES
dc.identifier.doi10.1038/s41467-018-03433-3-
dc.description.peerreviewedPeer reviewedes_ES
dc.relation.publisherversionhttps://doi.org/10.1038/s41467-018-03433-3es_ES
dc.identifier.e-issn2041-1723-
dc.rights.licensehttp://creativecommons.org/ licenses/by/4.0/es_ES
dc.contributor.funderInstitución Catalana de Investigación y Estudios Avanzadoses_ES
dc.contributor.funderFundació La Marató de TV3es_ES
dc.contributor.funderMinisterio de Sanidad, Servicios Sociales e Igualdad (España)es_ES
dc.contributor.funderMinisterio de Economía y Competitividad (España)es_ES
dc.contributor.funderCentro de Investigación Biomédica en Red Enfermedades Raras (España)es_ES
dc.contributor.funderEuropean Commissiones_ES
dc.contributor.funderFanconi Anemia Research Fundes_ES
dc.contributor.funderInstituto de Salud Carlos IIIes_ES
dc.contributor.funderAsociación Española Contra el Cánceres_ES
dc.contributor.funderGeneralitat de Catalunyaes_ES
dc.relation.csices_ES
oprm.item.hasRevisionno ko 0 false*
dc.identifier.funderhttp://dx.doi.org/10.13039/100002086es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100004587es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/100008666es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100003751es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100000780es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100002809es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100003329es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100003741es_ES
dc.contributor.orcidBrunet, Joan [0000-0003-1945-3512]es_ES
dc.contributor.orcidHuertas Sánchez, Pablo [0000-0002-1756-4449]es_ES
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