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dc.contributor.authorIzquierdo-Bouldstridge, Andreaes_ES
dc.contributor.authorBustillos, Albertoes_ES
dc.contributor.authorBonet-Costa, Carleses_ES
dc.contributor.authorAribau-Miralbés, Patriciaes_ES
dc.contributor.authorGarcía-Gomis, Danieles_ES
dc.contributor.authorDabad, Marces_ES
dc.contributor.authorEsteve-Codina, Annaes_ES
dc.contributor.authorPascual-Reguant, Lauraes_ES
dc.contributor.authorPeiró, Sandraes_ES
dc.contributor.authorEsteller, Maneles_ES
dc.contributor.authorMurtha, Matthewes_ES
dc.contributor.authorMillán-Ariño, Lluises_ES
dc.contributor.authorJordan, Albertes_ES
dc.date.accessioned2019-01-15T08:20:47Z-
dc.date.available2019-01-15T08:20:47Z-
dc.date.issued2017-11-16-
dc.identifier.citationNucleic Acids Research 45(20): 11622–11642 (2017)es_ES
dc.identifier.issn0305-1048-
dc.identifier.urihttp://hdl.handle.net/10261/174077-
dc.description.abstractHistone H1 has seven variants in human somatic cells and contributes to chromatin compaction and transcriptional regulation. Knock-down (KD) of each H1 variant in breast cancer cells results in altered gene expression and proliferation differently in a variant specific manner with H1.2 and H1.4 KDs being most deleterious. Here we show combined depletion of H1.2 and H1.4 has a strong deleterious effect resulting in a strong interferon (IFN) response, as evidenced by an up-regulation of many IFN-stimulated genes (ISGs) not seen in individual nor in other combinations of H1 variant KDs. Although H1 participates to repress ISG promoters, IFN activation upon H1.2 and H1.4 KD is mainly generated through the activation of the IFN response by cytosolic nucleic acid receptors and IFN synthesis, and without changes in histone modifications at induced ISG promoters. H1.2 and H1.4 co-KD also promotes the appearance of accessibility sites genome wide and, particularly, at satellites and other repeats. The IFN response may be triggered by the expression of noncoding RNA generated from heterochromatic repeats or endogenous retroviruses upon H1 KD. In conclusion, redundant H1-mediated silencing of heterochromatin is important to maintain cell homeostasis and to avoid an unspecific IFN response.es_ES
dc.description.sponsorshipSpanish Ministry of Economy and Competitiveness (MINECO) and European Regional Development Fund [BFU2014–52237-P]. A.B. received a predoctoral fellowship from SENESCYT from Ecuador. M.D. was recipient of a fellowship from MINECO [PTA2014– 09515-I]. A.E.-C. was funded by the RED-BIO project of the Spanish National Bioinformatics Institute (INB) [PT13/0001/0044]. The INB is funded by the Spanish National Health Institute Carlos III (ISCIII) and MINECO. Funding for open access charge: Spanish Ministry of Economy and Competitiveness (MINECO) and European Regional Development Fund [BFU2014-52237-P].es_ES
dc.language.isoenges_ES
dc.publisherOxford University Presses_ES
dc.relationMINECO/ICTI2013-2016/BFU2014–52237-Pes_ES
dc.relationMINECO/ICTI2013-2016/PTA2014–09515-Ies_ES
dc.relation.isversionofPublisher's versiones_ES
dc.rightsopenAccesses_ES
dc.titleHistone H1 depletion triggers an interferon response in cancer cells via activation of heterochromatic repeatses_ES
dc.typeartículoes_ES
dc.identifier.doi10.1093/nar/gkx746-
dc.description.peerreviewedPeer reviewedes_ES
dc.relation.publisherversionhttps://doi.org/10.1093/nar/gkx746es_ES
dc.identifier.e-issn1362-4962-
dc.rights.licensehttp://creativecommons.org/licenses/by-nc/4.0/es_ES
dc.contributor.funderMinisterio de Economía y Competitividad (España)es_ES
dc.contributor.funderEuropean Commissiones_ES
dc.contributor.funderSecretaría de Educación Superior, Ciencia, Tecnología e Innovación (Ecuador)es_ES
dc.contributor.funderInstituto Nacional de Bioinformática (España)es_ES
dc.contributor.funderInstituto de Salud Carlos IIIes_ES
dc.relation.csices_ES
oprm.item.hasRevisionno ko 0 false*
dc.identifier.funderhttp://dx.doi.org/10.13039/501100003329es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100000780es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100004299es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100004587es_ES
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