File Download
  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Cdk5 is involved in BDNF-stimulated dendritic growth in hippocampal neurons

TitleCdk5 is involved in BDNF-stimulated dendritic growth in hippocampal neurons
Authors
KeywordsAmino Acid Sequence
Animal Cell
Article
Cell Differentiation
Cell Growth
Cell Maturation
Cell Survival
Controlled Study
Dendritic Cell
Hippocampus
Mouse
Nerve Cell
Nonhuman
Protein Analysis
Protein Interaction
Protein Phosphorylation
Issue Date2007
PublisherPublic Library of Science. The Journal's web site is located at http://www.plosbiology.org/plosonline/?request=index-html
Citation
Plos Biology, 2007, v. 5 n. 4, p. 865-877 How to Cite?
AbstractNeurotrophins are key regulators of neuronal survival and differentiation during development. Activation of their cognate receptors, Trk receptors, a family of receptor tyrosine kinases (RTKs), is pivotal for mediating the downstream functions of neurotrophins. Recent studies reveal that cyclin-dependent kinase 5 (Cdk5), a serine/threonine kinase, may modulate RTK signaling through phosphorylation of the receptor. Given the abundant expression of both Cdk5 and Trk receptors in the nervous system, and their mutual involvement in the regulation of neuronal architecture and synaptic functions, it is of interest to investigate if Cdk5 may also modulate Trk signaling. In the current study, we report the identification of TrkB as a Cdk5 substrate. Cdk5 phosphorylates TrkB at Ser478 at the intracellular juxtamembrane region of TrkB. Interestingly, attenuation of Cdk5 activity or overexpression of a TrkB mutant lacking the Cdk5 phosphorylation site essentially abolishes brain-derived neurotrophic factor (BDNF)-triggered dendritic growth in primary hippocampal neurons. In addition, we found that Cdk5 is involved in BDNF-induced activation of Rho GTPase Cdc42, which is essential for BDNF-triggered dendritic growth. Our observations therefore reveal an unanticipated role of Cdk5 in TrkB-mediated regulation of dendritic growth through modulation of BDNF-induced Cdc42 activation. © 2007 Cheung et al.
Persistent Identifierhttp://hdl.handle.net/10722/145821
ISSN
2010 Impact Factor: 12.472
2015 SCImago Journal Rankings: 5.293
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorCheung, ZHen_HK
dc.contributor.authorChin, WHen_HK
dc.contributor.authorChen, Yen_HK
dc.contributor.authorNg, YPen_HK
dc.contributor.authorIp, NYen_HK
dc.date.accessioned2012-03-23T09:49:49Z-
dc.date.available2012-03-23T09:49:49Z-
dc.date.issued2007en_HK
dc.identifier.citationPlos Biology, 2007, v. 5 n. 4, p. 865-877en_HK
dc.identifier.issn1544-9173en_HK
dc.identifier.urihttp://hdl.handle.net/10722/145821-
dc.description.abstractNeurotrophins are key regulators of neuronal survival and differentiation during development. Activation of their cognate receptors, Trk receptors, a family of receptor tyrosine kinases (RTKs), is pivotal for mediating the downstream functions of neurotrophins. Recent studies reveal that cyclin-dependent kinase 5 (Cdk5), a serine/threonine kinase, may modulate RTK signaling through phosphorylation of the receptor. Given the abundant expression of both Cdk5 and Trk receptors in the nervous system, and their mutual involvement in the regulation of neuronal architecture and synaptic functions, it is of interest to investigate if Cdk5 may also modulate Trk signaling. In the current study, we report the identification of TrkB as a Cdk5 substrate. Cdk5 phosphorylates TrkB at Ser478 at the intracellular juxtamembrane region of TrkB. Interestingly, attenuation of Cdk5 activity or overexpression of a TrkB mutant lacking the Cdk5 phosphorylation site essentially abolishes brain-derived neurotrophic factor (BDNF)-triggered dendritic growth in primary hippocampal neurons. In addition, we found that Cdk5 is involved in BDNF-induced activation of Rho GTPase Cdc42, which is essential for BDNF-triggered dendritic growth. Our observations therefore reveal an unanticipated role of Cdk5 in TrkB-mediated regulation of dendritic growth through modulation of BDNF-induced Cdc42 activation. © 2007 Cheung et al.en_HK
dc.languageengen_US
dc.publisherPublic Library of Science. The Journal's web site is located at http://www.plosbiology.org/plosonline/?request=index-htmlen_HK
dc.relation.ispartofPLoS Biologyen_HK
dc.subjectAmino Acid Sequenceen_US
dc.subjectAnimal Cellen_US
dc.subjectArticleen_US
dc.subjectCell Differentiationen_US
dc.subjectCell Growthen_US
dc.subjectCell Maturationen_US
dc.subjectCell Survivalen_US
dc.subjectControlled Studyen_US
dc.subjectDendritic Cellen_US
dc.subjectHippocampusen_US
dc.subjectMouseen_US
dc.subjectNerve Cellen_US
dc.subjectNonhumanen_US
dc.subjectProtein Analysisen_US
dc.subjectProtein Interactionen_US
dc.subjectProtein Phosphorylationen_US
dc.titleCdk5 is involved in BDNF-stimulated dendritic growth in hippocampal neuronsen_HK
dc.typeArticleen_HK
dc.identifier.emailCheung, ZH:zelda@hku.hken_HK
dc.identifier.authorityCheung, ZH=rp01588en_HK
dc.description.naturepublished_or_final_versionen_US
dc.identifier.doi10.1371/journal.pbio.0050063en_HK
dc.identifier.pmid17341134-
dc.identifier.pmcidPMC1808488-
dc.identifier.scopuseid_2-s2.0-34247342131en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34247342131&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume5en_HK
dc.identifier.issue4en_HK
dc.identifier.spage865en_HK
dc.identifier.epage877en_HK
dc.identifier.eissn1545-7885-
dc.identifier.isiWOS:000245901500018-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridCheung, ZH=6507483375en_HK
dc.identifier.scopusauthoridChin, WH=10141627600en_HK
dc.identifier.scopusauthoridChen, Y=25927793500en_HK
dc.identifier.scopusauthoridNg, YP=7202471018en_HK
dc.identifier.scopusauthoridIp, NY=7005756760en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats