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dc.contributor.authorEgea Navarro, Joaquim
dc.contributor.authorEspinet Mestre, Carme
dc.contributor.authorSoler i Tatché, Rosa Ma.
dc.contributor.authorDolcet Roca, Xavier
dc.contributor.authorYuste Mateos, Víctor J. (Víctor José)
dc.contributor.authorEncinas Martín, Mario
dc.contributor.authorIglesias Durán, Montserrat
dc.contributor.authorRocamora Ibars, Nativitat
dc.contributor.authorComella i Carnicé, Joan Xavier
dc.date.accessioned2012-12-21T12:30:01Z
dc.date.available2012-12-21T12:30:01Z
dc.date.issued2001
dc.identifier.issn0021-9525
dc.identifier.urihttp://hdl.handle.net/10459.1/46380
dc.description.abstractIt has been reported that phosphoinositide 3-kinase (PI 3-kinase) and its downstream target, protein kinase B (PKB), play a central role in the signaling of cell survival triggered by neurotrophins (NTs). In this report, we have analyzed the involvement of Ca2+ and calmodulin (CaM) in the activation of the PKB induced by NTs. We have found that reduction of intracellular Ca2+ concentration or functional blockade of CaM abolished NGF-induced activation of PKB in PC12 cells. Similar results were obtained in cultures of chicken spinal cord motoneurons treated with brain-derived neurotrophic factor (BDNF). Moreover, CaM inhibition prevented the cell survival triggered by NGF or BDNF. This effect was counteracted by the transient expression of constitutive active forms of the PKB, indicating that CaM regulates NT-induced cell survival through the activation of the PKB. We have investigated the mechanisms whereby CaM regulates the activation of the PKB, and we have found that CaM was necessary for the proper generation and/or accumulation of the products of the PI 3-kinase in intact cells.ca_ES
dc.language.isoengca_ES
dc.publisherRockefeller University Pressca_ES
dc.relation.isformatofReproducció del document publicat a: https://doi.org/10.1083/jcb.200101023ca_ES
dc.relation.ispartofJournal of Cell Biology, 2001, vol. 154, núm. 3, p. 585–597ca_ES
dc.rights(c) Rockefeller University Press, 2001ca_ES
dc.subject.otherCalmodulinaca_ES
dc.subject.otherNeuronesca_ES
dc.subject.otherNeurobiologiaca_ES
dc.subject.otherMort cel·lularca_ES
dc.titleNeuronal survival induced by neurotrophins requires calmodulinca_ES
dc.typearticleca_ES
dc.identifier.idgrec005715
dc.type.versionpublishedVersionca_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccessca_ES
dc.identifier.doihttps://doi.org/10.1083/jcb.200101023


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