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dc.contributor.authorXifró, Xavier
dc.contributor.authorFalluel-Morel, Anthony
dc.contributor.authorMiñano Molina, Alfredo Jesús
dc.contributor.authorAubert, Nicolas
dc.contributor.authorFadó Andrés, Rut
dc.contributor.authorMalagelada, Cristina
dc.contributor.authorVaudry, David
dc.contributor.authorVaudry, Hubert
dc.contributor.authorGonzalez, Druno
dc.contributor.authorRodríguez-Álvarez, José
dc.date.accessioned2021-05-03T17:18:26Z
dc.date.available2021-05-03T17:18:26Z
dc.date.issued2006-03-10
dc.identifier.citationXifró, Xavier; Falluel-Morel, Anthony; Miñano, Alfredo [et al.]. N-methyl-DD-aspartate blocks activation of JNK and mitochondrial apoptotic pathway induced by potassium deprivation in cerebellar granule cells. Journal of Biological Chemistry, 2006, 281(10), p. 6801-6812. Disponible en: <https://www.sciencedirect.com/science/article/pii/S0021925819580413?via%3Dihub>. Fecha de acceso: 3 may. 2021. DOI: 10.1074/jbc.M504571200ca
dc.identifier.issn0021-9258ca
dc.identifier.urihttp://hdl.handle.net/20.500.12328/2514
dc.description.abstractDuring the postnatal development of cerebellum, lack of excitatory innervation from the mossy fibers results in cerebellar granule cell (CGC) apoptosis during the migration of the cells toward the internal granule cell layer. Accordingly, CGCs die by apoptosis when cultured in physiological KCl concentrations (5 mm; K5), and they survive in the presence of depolarizing conditions such as high KCl concentration (25 mm; K25) or N-methyl-d-aspartate (NMDA). We have recently shown that NMDA is able to exert a long lasting neuroprotective effect when added to immature (2 days in vitro) CGC cultures by inhibition of caspase-3 activity. Here we show that NMDA- and K25-mediated neuroprotection is associated with an increase in the levels of Bcl-2, an inhibition of K5-mediated increase in Bax, and the inhibition of the release of apoptogenic factors from mitochondria such as Smac/DIABLO and cytochrome c. Moreover, we have shown that similar effects are observed when c-Jun N-terminal kinases (JNKs) are inhibited and that treatment of CGC cultures with NMDA blocks K5-mediated JNK activation. These results allow us to postulate that the inhibition of JNK-mediated release of apoptogenic factors from mitochondria is involved in the NMDA protection from K5-mediated apoptosis of CGCs.en
dc.format.extent12ca
dc.language.isoengca
dc.publisherElsevierca
dc.relation.ispartofJournal of Biological Chemistryca
dc.relation.ispartofseries281;10
dc.rightsUnder a Creative Commons license. This is an Open Access article under the CC-BY License.en
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.subject.otherApoptosica
dc.subject.otherCervell -- Malaltiesca
dc.subject.otherPotassica
dc.subject.otherMitocondrisca
dc.subject.otherApoptosises
dc.subject.otherCerebro -- Enfermedadeses
dc.subject.otherPotasioes
dc.subject.otherMitocondriases
dc.subject.otherApoptosisen
dc.subject.otherBrain -- Diseasesen
dc.subject.otherPotassiumen
dc.subject.otherMitochondriaen
dc.titleN-methyl-DD-aspartate blocks activation of JNK and mitochondrial apoptotic pathway induced by potassium deprivation in cerebellar granule cellsen
dc.typeinfo:eu-repo/semantics/articleca
dc.description.versioninfo:eu-repo/semantics/publishedVersionca
dc.rights.accessLevelinfo:eu-repo/semantics/openAccess
dc.embargo.termscapca
dc.relation.projectIDrepo/grantAgreement/ES/1PN/SAF2001-1941ca
dc.subject.udc61ca
dc.identifier.doihttps://dx.doi.org/10.1074/jbc.M504571200ca


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Under a Creative Commons license. This is an Open Access article under the CC-BY License.
Except where otherwise noted, this item's license is described as https://creativecommons.org/licenses/by/4.0/