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Identificador persistente para citar o vincular este elemento: http://hdl.handle.net/10662/20226
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dc.contributor.authorMartin, Tamara P.-
dc.contributor.authorHortigón Vinagre, Maria Pura-
dc.contributor.authorFindlay, Jane E.-
dc.contributor.authorElliot, Christina-
dc.contributor.authorCurrie, Susan-
dc.contributor.authorBaillie, George-
dc.date.accessioned2024-02-07T10:48:40Z-
dc.date.available2024-02-07T10:48:40Z-
dc.date.issued2014-
dc.identifier.urihttp://hdl.handle.net/10662/20226-
dc.description.abstractPhosphorylated heat shock protein 20 (HSP20) is cardioprotective. Using human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) and a mouse model of pressure overload mediated hypertrophy, we show that peptide disruption of the HSP20-phosphodiesterase 4D (PDE4D) complex results in attenuation of action potential prolongation and protection against adverse cardiac remodelling. The later was evidenced by improved contractility, decreased heart weight to body weight ratio, and reduced interstitial and perivascular fibrosis. This study demonstrates that disruption of the specific HSP20-PDE4D interaction leads to attenuation of pathological cardiac remodellinges_ES
dc.description.sponsorshipThis work was supported by (Grant No: RG2610). G.S.B. is supported by MRC grant (MR/J007412/1). We are extremely grateful to Mr Graeme MacKenzie for technical assistance. MPH-V is recipient of a postdoctoral fellowship from Fundacion Alfonso Martin Escudero, Spain. GSB and SC conceived and designed the project, TPM, MPV-H, JEF and CE acquired and analyzed the data, TPM, GSB and SC wrote the paper.-
dc.format.extent5 p.es_ES
dc.format.mimetypeapplication/pdfen_US
dc.language.isoenges_ES
dc.publisherWiley-Blackwelles_ES
dc.rightsAtribución-NoComercial-SinDerivadas 4.0 Internacional-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/4.0/-
dc.subjectcAMPes_ES
dc.subjectPDE4Des_ES
dc.subjectHSP20es_ES
dc.subjectCardiac remodelinges_ES
dc.subjectCardiac hypertrophyes_ES
dc.subjectPeptide disruptiones_ES
dc.subjectRemodelación cardiaca-
dc.subjectHipertrofia cardiaca-
dc.subjectAlteración de péptidos-
dc.titleTargeted disruption of the heat shock protein 20-phosphodiesterase 4D (PDE4D) interaction protects against pathological cardiac remodelling in a mouse model of hypertrophyes_ES
dc.typearticlees_ES
dc.description.versionpeerReviewedes_ES
europeana.typeTEXTen_US
dc.rights.accessRightsopenAccesses_ES
dc.subject.unesco3205.01Cardiología-
europeana.dataProviderUniversidad de Extremadura. Españaes_ES
dc.identifier.bibliographicCitationMartin Tamara P., Hortigon-Vinagre Maria P., Findlay Jane E., Elliott Christina, Currie Susan and Baillie George S.(2014), Targeted disruption of the heat shock protein 20–phosphodiesterase 4D (PDE4D) interaction protects against pathological cardiac remodelling in a mouse model of hypertrophy, FEBS Open Bio, 4, doi: 10.1016/j.fob.2014.10.011-
dc.type.versionpublishedVersiones_ES
dc.contributor.affiliationUniversidad de Extremadura. Departamento de Bioquímica, Biología Molecular y Genéticaes_ES
dc.contributor.affiliationUniversity of Glasgow. UK-
dc.relation.publisherversionhttps://febs.onlinelibrary.wiley.com/doi/10.1016/j.fob.2014.10.011es_ES
dc.identifier.doi10.1016/j.fob.2014.10.011-
dc.identifier.publicationtitleFEBS Open Bioes_ES
dc.identifier.publicationfirstpage923es_ES
dc.identifier.publicationlastpage927es_ES
dc.identifier.publicationvolume4es_ES
dc.identifier.orcid0000-0001-5531-1779es_ES
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