Bcl-X-L inhibits Bax-induced alterations in mitochondrial respiration and calcium release

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dc.contributor.authorTeles, Alessandra Vaz Fernandes Fiuza [UNIFESP]
dc.contributor.authorUreshino, Rodrigo Portes [UNIFESP]
dc.contributor.authorDorta, Daniel Junqueira [UNIFESP]
dc.contributor.authorLopes, Guiomar Silva [UNIFESP]
dc.contributor.authorHsu, Yi-Te
dc.contributor.authorSmaili, Soraya Soubhi [UNIFESP]
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.contributor.institutionMed Univ S Carolina
dc.date.accessioned2016-01-24T13:51:41Z
dc.date.available2016-01-24T13:51:41Z
dc.date.issued2008-09-12
dc.description.abstractApoptosis is a natural cell elimination process involved in a number of physiological and pathological events. This process can be regulated by members of the Bcl-2 family. Bax, a pro-apoptotic member of this family, accelerates cell death, while the pro-survival member, Bcl-X-L, can antagonize the pro-apoptotic function of Bax to promote cell survival. in the present study, we have evaluated the effect of Bcl-X-L on Bax-induced alterations in mitochondrial. respiration and calcium release. We found that in primary cultured astrocytes, recombinant Bcl-X-L is able to antagonize Bax-induced decrease in mitochondrial respiration and increase in mitochondrial. calcium release. in addition, we found that Bcl-X-L can lower the calcium store in the endoplasmic reticulum, thus limiting potential calcium flux induced by apoptosis. This regulation of calcium flux by Bcl-X-L may represent an important mechanism by which this protein promotes cell survival. (c) 2008 Elsevier Ireland Ltd. All rights reserved.en
dc.description.affiliationUniversidade Federal de São Paulo, Dept Farmacol, BR-04044020 São Paulo, Brazil
dc.description.affiliationMed Univ S Carolina, Dept Biochem & Mol Biol, Charleston, SC 29425 USA
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Farmacol, BR-04044020 São Paulo, Brazil
dc.description.sourceWeb of Science
dc.description.sponsorshipNIH
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description.sponsorshipIDNIH: NS40932
dc.format.extent96-99
dc.identifierhttps://dx.doi.org/10.1016/j.neulet.2008.06.073
dc.identifier.citationNeuroscience Letters. Clare: Elsevier B.V., v. 442, n. 2, p. 96-99, 2008.
dc.identifier.doi10.1016/j.neulet.2008.06.073
dc.identifier.issn0304-3940
dc.identifier.urihttps://repositorio.unifesp.br/handle/11600/30904
dc.identifier.wosWOS:000258909500004
dc.language.isoeng
dc.publisherElsevier B.V.
dc.relation.ispartofNeuroscience Letters
dc.rightsinfo:eu-repo/semantics/restrictedAccess
dc.rights.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.subjectBcl-X-Len
dc.subjectBaxen
dc.subjectCalciumen
dc.subjectApoptosisen
dc.subjectMitochondriaen
dc.subjectRespiratory chainen
dc.subjectATPen
dc.subjectADPen
dc.subjectCell deathen
dc.titleBcl-X-L inhibits Bax-induced alterations in mitochondrial respiration and calcium releaseen
dc.typeinfo:eu-repo/semantics/article
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