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dc.contributor.authorEncinas Martín, Mario
dc.contributor.authorRozen, Esteban Javier
dc.contributor.authorDolcet Roca, Xavier
dc.contributor.authorJain, Sanjay
dc.contributor.authorComella i Carnicé, Joan Xavier
dc.contributor.authorMilbrandt, Jeffrey
dc.contributor.authorJohnson, Eugene M.
dc.description.abstractWe analyzed the survival responses and downstream signaling elicited by GDNF on sympathetic neurons from different Ret knockin mice. Lack of tyrosine 1062, a multidocking site in Ret, completely prevented GDNF-mediated survival. Importantly lack of tyrosine 981, although abrogating Akt phosphorylation, had no effect on neuronal survival, indicating that the PI 3-K/Akt pathway is not necessary for survival of sympathetic neurons. In contrast, silencing of B-Raf completely prevented not only GDNF-mediated but also NGF-mediated cell survival, independently of MEK-1/2. We identified IKKs as the main effectors of the protective effects of B-Raf. First, BRaf interacted with and activated IKKs. Second, knockdown of IKKs reversed the protection afforded by a constitutively active form of B-Raf. Third, knockdown of IKKs prevented both NGF- and GDNF-mediated survival. In conclusion, our data delineate a novel survival pathway for sympathetic neurons linking B-Raf to IKKs, independently of both PI 3-K and MEK-1/2 pathways.ca_ES
dc.publisherNature Publishing Groupca_ES
dc.relation.isformatofReproducció del document publicat a
dc.relation.ispartofCell Death and Differentiation, 2008, vol. 15, núm. 9, p. 1510-1521ca_ES
dc.rights(c) ADMC Associazione Differenziamento e Morte Cellulare, 2008
dc.subject.otherSistema nerviós--Malaltiesca_ES
dc.titleAnalysis of Ret knockin mice reveals a critical role for IKKs, but not PI 3-K, in neurotrophic factor-induced survival of sympathetic neurons.ca_ES

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(c) ADMC Associazione Differenziamento e Morte Cellulare, 2008
Except where otherwise noted, this item's license is described as (c) ADMC Associazione Differenziamento e Morte Cellulare, 2008