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Authordc.contributor.authorEisner, Verónica 
Authordc.contributor.authorQuiroga, Clara 
Authordc.contributor.authorCriollo Céspedes, Alfredo 
Authordc.contributor.authorEltit Ortega, José Miguel 
Authordc.contributor.authorChiong Lay, Mario 
Authordc.contributor.authorParra, Valentina 
Authordc.contributor.authorHidalgo, Karla 
Authordc.contributor.authorToro, Barbra 
Authordc.contributor.authorDíaz Araya, Guillermo 
Authordc.contributor.authorLavandero González, Sergio 
Admission datedc.date.accessioned2018-12-20T15:10:05Z
Available datedc.date.available2018-12-20T15:10:05Z
Publication datedc.date.issued2006
Cita de ítemdc.identifier.citationFEBS Letters, Volumen 580, Issue 14, 2018, Pages 3469-3476
Identifierdc.identifier.issn00145793
Identifierdc.identifier.other10.1016/j.febslet.2006.05.023
Identifierdc.identifier.urihttps://repositorio.uchile.cl/handle/2250/158138
Abstractdc.description.abstractNFκB is a participant in the process whereby cells adapt to stress. We have evaluated the activation of NFκB pathway by hyperosmotic stress in cultured cardiomyocytes and its role in the activation of caspase and cell death. Exposure of cultured rat cardiomyocytes to hyperosmotic conditions induced phosphorylation of IKKα/β as well as degradation of IκBα. All five members of the NFκB family were identified in cardiomyocytes. Analysis of the subcellular distribution of NFκB isoforms in response to hyperosmotic stress showed parallel migration of p65 and RelB from the cytosol to the nucleus. Measurement of the binding of NFκB to the consensus DNA κB-site binding by EMSA revealed an oscillatory profile with maximum binding 1, 2 and 6 h after initiation of the hyperosmotic stress. Supershift analysis revealed that p65 and RelB (but not p50, p52 or cRel) were involved in the binding of NFκB to DNA. Hyperosmotic stress also resulted in activation of the NFκB-lux reporter gene, transient acti
Lenguagedc.language.isoen
Type of licensedc.rightsAttribution-NonCommercial-NoDerivs 3.0 Chile
Link to Licensedc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/cl/
Sourcedc.sourceFEBS Letters
Keywordsdc.subjectApoptosis
Keywordsdc.subjectCaspase
Keywordsdc.subjectCell death
Keywordsdc.subjectNFκB
Keywordsdc.subjectOsmotic stress
Títulodc.titleHyperosmotic stress activates p65/RelB NFκB in cultured cardiomyocytes with dichotomic actions on caspase activation and cell death
Document typedc.typeArtículo de revista
Catalogueruchile.catalogadorSCOPUS
Indexationuchile.indexArtículo de publicación SCOPUS
uchile.cosechauchile.cosechaSI


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Attribution-NonCommercial-NoDerivs 3.0 Chile
Except where otherwise noted, this item's license is described as Attribution-NonCommercial-NoDerivs 3.0 Chile