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dc.contributor.authorShahbazi, Marta N
dc.contributor.authorPeña-Jiménez, Daniel 
dc.contributor.authorAntonucci, Francesca
dc.contributor.authorDrosten, Matthias 
dc.contributor.authorPerez-Moreno, Mirna Alicia 
dc.date.accessioned2019-10-14T12:18:09Z
dc.date.available2019-10-14T12:18:09Z
dc.date.issued2017-02-15
dc.identifier.citationJ Cell Sci. 2017;130(4):683-688es_ES
dc.identifier.issn0021-9533es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/8495
dc.description.abstractEpidermal homeostasis is tightly controlled by a balancing act of self-renewal or terminal differentiation of proliferating basal keratinocytes. An increase in DNA content as a consequence of a mitotic block is a recognized mechanism underlying keratinocyte differentiation, but the molecular mechanisms involved in this process are not yet fully understood. Using cultured primary keratinocytes, here we report that the expression of the mammalian microtubule and kinetochore-associated protein Clasp2 is intimately associated with the basal proliferative makeup of keratinocytes, and its deficiency leads to premature differentiation. Clasp2-deficient keratinocytes exhibit increased centrosomal numbers and numerous mitotic alterations, including multipolar spindles and chromosomal misalignments that overall result in mitotic stress and a high DNA content. Such mitotic block prompts premature keratinocyte differentiation in a p53-dependent manner in the absence of cell death. Our findings reveal a new role for Clasp2 in governing keratinocyte undifferentiated features and highlight the presence of surveillance mechanisms that prevent cell cycle entry in cells that have alterations in the DNA content.es_ES
dc.description.sponsorshipThis work was supported by grants from the Spanish Ministerio de Economia y Competitividad (MINECO) [BFU2012-33910 and BFU2015-71376-R (MINECO/ European Regional Development Fund (ERDF), European Union) to M.P.-M.]. Deposited in PMC for immediate release.es_ES
dc.language.isoenges_ES
dc.publisherThe Company of Biologists es_ES
dc.type.hasVersionVoRes_ES
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.subjectCell cyclees_ES
dc.subjectClasp2es_ES
dc.subjectDifferentiationes_ES
dc.subjectKeratinocyteses_ES
dc.subjectMicrotubuleses_ES
dc.subject.meshAnimals es_ES
dc.subject.meshCell Line, Transformed es_ES
dc.subject.meshCells, Cultured es_ES
dc.subject.meshDNA Damage es_ES
dc.subject.meshGene Knockdown Techniques es_ES
dc.subject.meshHumans es_ES
dc.subject.meshKeratinocytes es_ES
dc.subject.meshMice, Inbred C57BL es_ES
dc.subject.meshMicrotubule-Associated Proteins es_ES
dc.subject.meshTumor Suppressor Protein p53 es_ES
dc.subject.meshCell Differentiation es_ES
dc.subject.meshEpidermal Cells es_ES
dc.subject.meshMitosis es_ES
dc.titleClasp2 ensures mitotic fidelity and prevents differentiation of epidermal keratinocyteses_ES
dc.typejournal articlees_ES
dc.rights.licenseAtribución-NoComercial-CompartirIgual 4.0 Internacional*
dc.identifier.pubmedID28069833es_ES
dc.format.volume130es_ES
dc.format.number4es_ES
dc.format.page683-688es_ES
dc.identifier.doi10.1242/jcs.194787es_ES
dc.contributor.funderMinisterio de Economía y Competitividad (España) 
dc.description.peerreviewedes_ES
dc.identifier.e-issn1477-9137es_ES
dc.relation.publisherversionhttps://doi.org/10.1242/jcs.194787.es_ES
dc.identifier.journalJournal of cell sciencees_ES
dc.repisalud.institucionCNIOes_ES
dc.repisalud.orgCNIOCNIO::Grupos de investigación::Antiguos CNIOes_ES
dc.relation.projectIDinfo:eu_repo/grantAgreement/ES/BFU2012-33910es_ES
dc.relation.projectIDinfo:eu_repo/grantAgreement/ES/BFU2015-71376-Res_ES
dc.rights.accessRightsopen accesses_ES


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Atribución-NoComercial-CompartirIgual 4.0 Internacional
This item is licensed under a: Atribución-NoComercial-CompartirIgual 4.0 Internacional