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dc.creatorÁlvarez Quilón, Alejandroes
dc.creatorSerrano Benítez, Almudenaes
dc.creatorAriel Lieberman, Jennaes
dc.creatorQuintero, Cristinaes
dc.creatorSánchez Gutiérrez, Danieles
dc.creatorEscudero Cuadrado, Luis Maríaes
dc.creatorCortés Ledesma, Felipees
dc.date.accessioned2017-03-29T11:28:27Z
dc.date.available2017-03-29T11:28:27Z
dc.date.issued2014
dc.identifier.issn2041-1723es
dc.identifier.urihttp://hdl.handle.net/11441/56529
dc.description.abstractAtaxia telangiectasia is caused by mutations in ATM and represents a paradigm for cancer predisposition and neurodegenerative syndromes linked to deficiencies in the DNA-damage response. The role of ATM as a key regulator of signalling following DNA double-strand breaks (DSBs) has been dissected in extraordinary detail, but the impact of this process on DSB repair still remains controversial. Here we develop novel genetic and molecular tools to modify the structure of DSB ends and demonstrate that ATM is indeed required for efficient and accurate DSB repair, preventing cell death and genome instability, but exclusively when the ends are irreversibly blocked. We therefore identify the nature of ATM involvement in DSB repair, presenting blocked DNA ends as a possible pathogenic trigger of ataxia telangiectasia and related disorders.es
dc.formatapplication/pdfes
dc.language.isoenges
dc.publisherNature Publishing Groupes
dc.relation.ispartofNature Communications, 5, 3347-1-3347-10.es
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.titleATM specifically mediates repair of double-strand breaks with blocked DNA endses
dc.typeinfo:eu-repo/semantics/articlees
dc.type.versioninfo:eu-repo/semantics/publishedVersiones
dc.rights.accessrightsinfo:eu-repo/semantics/openAccesses
dc.contributor.affiliationUniversidad de Sevilla. Departamento de Biología Celulares
dc.relation.publisherversion10.1038/ncomms4347es
dc.identifier.doihttp://dx.doi.org/10.1038/ncomms4347es
idus.format.extent11 p.es
dc.journaltitleNature Communicationses
dc.publication.volumen5es
dc.publication.initialPage3347-1es
dc.publication.endPage3347-10es

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Attribution-NonCommercial-NoDerivatives 4.0 Internacional
Except where otherwise noted, this item's license is described as: Attribution-NonCommercial-NoDerivatives 4.0 Internacional