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dc.contributor.authorEgea Navarro, Joaquim
dc.contributor.authorVig Nissen, Ulla
dc.contributor.authorDufour, Audrey
dc.contributor.authorSahin, Mustafa
dc.contributor.authorGreer, Paul
dc.contributor.authorKullander, Klas
dc.contributor.authorMrsic-Flogel, Thomas D.
dc.contributor.authorGreenberg, Michael E.
dc.contributor.authorKiehn, Ole
dc.contributor.authorVanderhaeghen, Pierre
dc.contributor.authorKlein, Rüdiger
dc.date.accessioned2016-05-20T07:58:24Z
dc.date.issued2005
dc.identifier.issn0896-6273
dc.identifier.urihttp://hdl.handle.net/10459.1/57064
dc.description.abstractSignaling by receptor tyrosine kinases (RTKs) is mediated by their intrinsic kinase activity. Typically, kinase-activating mutations result in ligand-independent signaling and gain-of-function phenotypes. Like other RTKs, Ephs require kinase activity to signal, but signaling by Ephs in vitro also requires clustering by their membrane bound ephrin ligands. The relative importance of Eph kinase activity and clustering for in vivo functions is unknown. We find that knockin mice expressing a mutant form of EphA4 (EphA4EE), whose kinase is constitutively activated in the absence of ephrinB ligands, are deficient in the development of thalamocortical projections and some aspects of central pattern generator rhythmicity. Surprisingly, other functions of EphA4 were regulated normally by EphA4EE, including midline axon guidance, hindlimb locomotion, in vitro growth cone collapse, and phosphorylation of ephexin1. These results suggest that signaling of Eph RTKs follows a multistep process of induced kinase activity and higher-order clustering different from RTKs responding to soluble ligands.ca_ES
dc.language.isoengca_ES
dc.publisherElsevierca_ES
dc.relation.isformatofReproducció del document publicat a https://doi.org/10.1016/j.neuron.2005.06.029ca_ES
dc.relation.ispartofNeuron, 2005, vol, 47, núm 4, p. 515-528ca_ES
dc.rights(c) Elsevier Inc., 2005ca_ES
dc.titleRegulation of EphA4 Kinase Activity Is Required for a Subset of Axon Guidance Decisions Suggesting a Key Role for Receptor Clustering in Eph Functionca_ES
dc.typearticleca_ES
dc.identifier.idgrec017843
dc.type.versionpublishedVersionca_ES
dc.rights.accessRightsinfo:eu-repo/semantics/restrictedAccessca_ES
dc.identifier.doihttps://doi.org/10.1016/j.neuron.2005.06.029
dc.date.embargoEndDate2025-01-01


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