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dc.contributor.authorCauseret, F.
dc.contributor.authorJacobs, T.
dc.contributor.authorTerao, M.
dc.contributor.authorHeath, O.
dc.contributor.authorHoshino, M.
dc.contributor.authorNikolic, Margareta
dc.date.accessioned2013-09-17T10:30:17Z
dc.date.available2013-09-17T10:30:17Z
dc.date.issued2007-11-01
dc.identifier.citationCauseret , F , Jacobs , T , Terao , M , Heath , O , Hoshino , M & Nikolic , M 2007 , ' Neurabin-I is phosphorylated by Cdk5 : Implications for neuronal morphogenesis and cortical migration ' , Molecular Biology of the Cell , vol. 18 , no. 11 , pp. 4327-4342 . https://doi.org/10.1091/mbc.E07-04-0372
dc.identifier.issn1059-1524
dc.identifier.otherPURE: 1743799
dc.identifier.otherPURE UUID: aaedf8cd-604a-4143-90b2-26277a107d6e
dc.identifier.otherScopus: 35848935639
dc.identifier.urihttp://hdl.handle.net/2299/11605
dc.descriptionMEDLINE® is the source for the MeSH terms of this document.
dc.description.abstractThe correct morphology and migration of neurons, which is essential for the normal development of the nervous system, is enabled by the regulation of their cytoskeletal elements. We reveal that Neurabin-I, a neuronal-specific F-actin-binding protein, has an essential function in the developing forebrain. We show that gain and loss of Neurabin-I expression affect neuronal morphology, neurite outgrowth, and radial migration of differentiating cortical and hippocampal neurons, suggesting that tight regulation of Neurabin-I function is required for normal forebrain development. Importantly, loss of Neurabin-I prevents pyramidal neurons from migrating into the cerebral cortex, indicating its essential role during early stages of corticogenesis. We demonstrate that in neurons Rac1 activation is affected by the expression levels of Neurabin-I. Furthermore, the Cdk5 kinase, a key regulator of neuronal migration and morphology, directly phosphorylates Neurabin-I and controls its association with F-actin. Mutation of the Cdk5 phosphorylation site reduces the phenotypic consequences of Neurabin-I overexpression both in vitro and in vivo, suggesting that Neurabin-I function depends, at least in part, on its phosphorylation status. Together our findings provide new insight into the signaling pathways responsible for controlled changes of the F-actin cytoskeleton that are required for normal development of the forebrain.en
dc.format.extent16
dc.language.isoeng
dc.relation.ispartofMolecular Biology of the Cell
dc.titleNeurabin-I is phosphorylated by Cdk5 : Implications for neuronal morphogenesis and cortical migrationen
dc.contributor.institutionSchool of Life and Medical Sciences
dc.contributor.institutionHealth & Human Sciences Research Institute
dc.contributor.institutionDepartment of Human and Environmental Sciences
dc.description.statusPeer reviewed
dc.identifier.urlhttp://www.scopus.com/inward/record.url?scp=35848935639&partnerID=8YFLogxK
dc.relation.schoolSchool of Life and Medical Sciences
dcterms.dateAccepted2007-11-01
rioxxterms.versionofrecordhttps://doi.org/10.1091/mbc.E07-04-0372
rioxxterms.typeJournal Article/Review
herts.preservation.rarelyaccessedtrue


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