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dc.contributor.authorSayas, C. Laura
dc.contributor.authorMedina, Miguel
dc.contributor.authorCuadros, Raquel
dc.contributor.authorOllá, Ivanna
dc.contributor.authorGarcía García-Esquinas, Esther 
dc.contributor.authorPérez Martínez, María Mar 
dc.contributor.authorFerrer, Isidro
dc.contributor.authorHernández Pérez, Félix 
dc.contributor.authorAvila, Jesús
dc.contributor.otherUAM. Departamento de Anatomía, Histología y Neurocienciaes_ES
dc.date.accessioned2019-08-14T14:19:14Z
dc.date.available2019-08-14T14:19:14Z
dc.date.issued2019-01-22
dc.identifier.citationPLoS ONE 14.1 (2019): e0210864en_US
dc.identifier.issn1932-6203 (online)es_ES
dc.identifier.urihttp://hdl.handle.net/10486/688387
dc.description.abstractFor unknown reasons, humans appear to be particular susceptible to developing tau pathology leading to neurodegeneration. Transgenic mice are still undoubtedly the most popular and extensively used animal models for studying Alzheimer’s disease and other tauopathies. While these murine models generally overexpress human tau in the mouse brain or specific brain regions, there are differences between endogenous mouse tau and human tau protein. Among them, a main difference between human and mouse tau is the presence of a short motif spanning residues 18 to 28 in the human tau protein that is missing in murine tau, and which could be at least partially responsible for that different susceptibility across species. Here we report novel data using affinity chromatography analysis indicating that the sequence containing human tau residues 18 to 28 acts a binding motif for End Binding proteins and that this interaction could facilitate tau secretion to the extracellular space.es_ES
dc.description.sponsorshipThis study was funded by grants from the Spanish Ministry of Economy and Competitiveness (SAF-2014-53040-P (Jesús Ávila), SAF2016-78603-R (Miguel Medina) and BFU2016-77885-P (Félix Hernández), the Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED, ISCIII) (Jesús Ávila). Institutional grants from the Fundación Ramón Areces and Banco Santander to the CBMSO are also acknowledgeden_US
dc.format.extent13 pag.es_ES
dc.format.mimetypeapplication/pdfen
dc.language.isospaen
dc.publisherPublic Library of Scienceen_US
dc.relation.ispartofPLos ONEen_US
dc.rights© 2019 Sayas et al.es_ES
dc.subject.otherNeurodegenerationen_US
dc.subject.otherAlzheimer’s diseaseen_US
dc.subject.otherProteinen_US
dc.subject.otherBrainen_US
dc.subject.otherChromatography analysisen_US
dc.titleRole of tau N-terminal motif in the secretion of human tau by end binding proteinsen_US
dc.typearticleen
dc.subject.ecienciaMedicinaes_ES
dc.relation.publisherversionhttps://doi.org/10.1371/journal.pone.0210864es_ES
dc.identifier.doi10.1371/journal.pone.0210864es_ES
dc.identifier.publicationfirstpagee0210864-1es_ES
dc.identifier.publicationissue1es_ES
dc.identifier.publicationlastpagee0210864-14es_ES
dc.identifier.publicationvolume14es_ES
dc.type.versioninfo:eu-repo/semantics/publishedVersionen
dc.rights.ccReconocimientoes_ES
dc.rights.accessRightsopenAccessen
dc.authorUAMPérez Martínez, María Mar (261357)
dc.facultadUAMFacultad de Medicina


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