Please use this identifier to cite or link to this item: http://hdl.handle.net/10553/50563
DC FieldValueLanguage
dc.contributor.authorTorres, Fernandoen_US
dc.contributor.authorQuintana, Joseen_US
dc.contributor.authorDíaz, Jesús G.en_US
dc.contributor.authorCarmona, Armando J.en_US
dc.contributor.authorEstévez, Franciscoen_US
dc.contributor.otherDiaz, Jesus-
dc.contributor.otherQuintana, Jose-
dc.contributor.otherEstevez, Francisco-
dc.contributor.otherTorres Andon, Fernando-
dc.date.accessioned2018-11-24T17:01:31Z-
dc.date.available2018-11-24T17:01:31Z-
dc.date.issued2008en_US
dc.identifier.issn1360-8185en_US
dc.identifier.urihttp://hdl.handle.net/10553/50563-
dc.description.abstractIn the present study we demonstrated that the flavonoid derivative trifolin acetate (TA), obtained by acetylation of naturally occurring trifolin, induces apoptosis. Associated downstream signaling events were also investigated. TA-induced cell death was prevented by the non-specific caspase inhibitor z-VAD-fmk and reduced by the presence of the selective caspase inhibitors z-LEHD-fmk (caspase-9), z-DEVD-fmk (caspase-3) and z-VEID-fmk (caspase-6). The apoptotic effect of TA was associated with (i) the release of cytochrome c from mitochondria which was not accompanied by dissipation of the mitochondrial membrane potential (Delta Psi(m)), (ii) the activation of the mitogen-activated protein kinases (MAPKs) pathway and (iii) abrogated by the over-expression of Bcl-2 or Bcl-x(L). TA-induced cell death was attenuated by inhibition of extracellular signal-regulated kinases (ERK) 1/2 with U0126 and inhibition of p38(MAPK) with SB203580. In contrast, inhibition of c-Jun NH2-terminal kinase (JNK) by SP600125 significantly enhanced apoptosis. Although reactive oxygen species (ROS) increased in response to TA, this did not seem to play a pivotal role in the apoptotic process since different anti-oxidants were unable to provide cell protection. The present study demonstrates that TA-induced cell death is mediated by an intrinsic-dependent apoptotic event involving mitochondria and MAPK, and through a mechanism independent of ROS generation.en_US
dc.languagespaen_US
dc.publisher1360-8185
dc.relationNuevos Compuestos Antileucémicosen_US
dc.relation.ispartofApoptosis : an international journal on programmed cell deathen_US
dc.sourceApoptosis[ISSN 1360-8185],v. 13, p. 716-728en_US
dc.subject.otherN-Terminal-Kinase
dc.subject.otherJun Nh2-Terminal Kinase
dc.subject.otherProtein-Kinase
dc.subject.otherInduced Apoptosis
dc.subject.otherCytochrome-C
dc.subject.otherPoly(Adp-Ribose) Polymerase
dc.subject.otherMediated Apoptosis
dc.subject.otherSignaling Pathways
dc.subject.otherCarcinoma Cells
dc.subject.otherCycle Arrest
dc.titleTrifolin acetate-induced cell death in human leukemia cells is dependent on caspase-6 and activates the MAPK pathwayen_US
dc.typeinfo:eu-repo/semantics/Articleen_US
dc.typeArticleen_US
dc.identifier.doi10.1007/s10495-008-0202-0en_US
dc.identifier.scopus42149184054-
dc.identifier.isi000255030400011-
dcterms.isPartOfApoptosis
dcterms.sourceApoptosis[ISSN 1360-8185],v. 13 (5), p. 716-728
dc.contributor.authorscopusid55366045300-
dc.contributor.authorscopusid8681043500-
dc.contributor.authorscopusid7401604406-
dc.contributor.authorscopusid23968598700-
dc.contributor.authorscopusid7003810011-
dc.description.lastpage728en_US
dc.description.firstpage716en_US
dc.relation.volume13en_US
dc.type2Artículoen_US
dc.identifier.wosWOS:000255030400011-
dc.contributor.daisngid34941095-
dc.contributor.daisngid2952604-
dc.contributor.daisngid128315-
dc.contributor.daisngid356785-
dc.contributor.daisngid4617455-
dc.contributor.daisngid384944-
dc.identifier.investigatorRIDL-6099-2014-
dc.identifier.investigatorRIDK-5709-2014-
dc.identifier.investigatorRIDK-5125-2014-
dc.identifier.investigatorRIDD-5184-2009-
dc.contributor.wosstandardWOS:Torres, F-
dc.contributor.wosstandardWOS:Quintana, J-
dc.contributor.wosstandardWOS:Diaz, JG-
dc.contributor.wosstandardWOS:Carmona, AJ-
dc.contributor.wosstandardWOS:Estevez, F-
dc.date.coverdateMayo 2008en_US
dc.identifier.ulpgces
dc.description.jcr3,971
dc.description.jcrqQ2
dc.description.scieSCIE
item.grantfulltextnone-
item.fulltextSin texto completo-
crisitem.project.principalinvestigatorEstévez Rosas, Francisco Jesús-
crisitem.author.deptGIR Bioquímica Farmacológica-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.deptDepartamento de Bioquímica y Biología Molecular, Fisiología, Genética e Inmunología.-
crisitem.author.deptGIR Bioquímica Farmacológica-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.deptDepartamento de Bioquímica y Biología Molecular, Fisiología, Genética e Inmunología.-
crisitem.author.orcid0000-0001-8225-4538-
crisitem.author.orcid0000-0002-9728-2774-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.fullNameQuintana Aguiar, José Martín-
crisitem.author.fullNameEstévez Rosas, Francisco Jesús-
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