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Article: Cdk5: Mediator of neuronal death and survival

TitleCdk5: Mediator of neuronal death and survival
Authors
KeywordsChemicals And Cas Registry Numbers: Cdk5 Protein, Human, Ec 2.7.1.37
Cdk5 Protein, Mouse, Ec 2.7.1.37
Cyclin-Dependent Kinase 5, Ec 2.7.1.37
Cyclin-Dependent Kinases, Ec 2.7.1.37
Nerve Tissue Proteins
Neuronal Cdk5 Activator (P25-P35)
Oncogene Proteins V-Erbb
Proto-Oncogene Proteins C-Jun
Issue Date2004
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/neulet
Citation
Neuroscience Letters, 2004, v. 361 n. 1-3, p. 47-51 How to Cite?
AbstractCdk5 (cyclin-dependent kinase 5) is a serine/threonine kinase implicated to play pivotal roles in neuronal development. Recently, its potential involvement as a regulator of neuronal death and survival has attracted considerable interests. Importantly, increasing evidence has linked Cdk5 to the etiopathology of neurodegenerative diseases such as Alzheimer's disease and amyotrophic lateral sclerosis. Here we summarize the recent findings on Cdk5 not only as an important participant in neuronal death, but also a key player in neuronal survival. Elucidating the mechanisms of regulation of Cdk5 and its downstream signaling might prove to be crucial in the therapeutic treatment of neurodegenerative diseases. © 2003 Elsevier Ireland Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/145827
ISSN
2015 Impact Factor: 2.107
2015 SCImago Journal Rankings: 1.035
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorCheung, ZHen_HK
dc.contributor.authorIp, NYen_HK
dc.date.accessioned2012-03-23T09:49:51Z-
dc.date.available2012-03-23T09:49:51Z-
dc.date.issued2004en_HK
dc.identifier.citationNeuroscience Letters, 2004, v. 361 n. 1-3, p. 47-51en_HK
dc.identifier.issn0304-3940en_HK
dc.identifier.urihttp://hdl.handle.net/10722/145827-
dc.description.abstractCdk5 (cyclin-dependent kinase 5) is a serine/threonine kinase implicated to play pivotal roles in neuronal development. Recently, its potential involvement as a regulator of neuronal death and survival has attracted considerable interests. Importantly, increasing evidence has linked Cdk5 to the etiopathology of neurodegenerative diseases such as Alzheimer's disease and amyotrophic lateral sclerosis. Here we summarize the recent findings on Cdk5 not only as an important participant in neuronal death, but also a key player in neuronal survival. Elucidating the mechanisms of regulation of Cdk5 and its downstream signaling might prove to be crucial in the therapeutic treatment of neurodegenerative diseases. © 2003 Elsevier Ireland Ltd. All rights reserved.en_HK
dc.languageengen_US
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/neuleten_HK
dc.relation.ispartofNeuroscience Lettersen_HK
dc.subjectChemicals And Cas Registry Numbers: Cdk5 Protein, Human, Ec 2.7.1.37en_US
dc.subjectCdk5 Protein, Mouse, Ec 2.7.1.37en_US
dc.subjectCyclin-Dependent Kinase 5, Ec 2.7.1.37en_US
dc.subjectCyclin-Dependent Kinases, Ec 2.7.1.37en_US
dc.subjectNerve Tissue Proteinsen_US
dc.subjectNeuronal Cdk5 Activator (P25-P35)en_US
dc.subjectOncogene Proteins V-Erbben_US
dc.subjectProto-Oncogene Proteins C-Junen_US
dc.subject.meshAnimalsen_HK
dc.subject.meshCell Death - geneticsen_HK
dc.subject.meshCell Survival - geneticsen_HK
dc.subject.meshCyclin-Dependent Kinase 5en_HK
dc.subject.meshCyclin-Dependent Kinases - genetics - metabolismen_HK
dc.subject.meshHumansen_HK
dc.subject.meshMiceen_HK
dc.subject.meshNerve Tissue Proteins - genetics - metabolismen_HK
dc.subject.meshNeurodegenerative Diseases - enzymology - genetics - physiopathologyen_HK
dc.subject.meshNeurons - enzymology - metabolismen_HK
dc.subject.meshOncogene Proteins v-erbB - genetics - metabolismen_HK
dc.subject.meshProto-Oncogene Proteins c-jun - genetics - metabolismen_HK
dc.subject.meshSignal Transduction - geneticsen_HK
dc.titleCdk5: Mediator of neuronal death and survivalen_HK
dc.typeArticleen_HK
dc.identifier.emailCheung, ZH:zelda@hku.hken_HK
dc.identifier.authorityCheung, ZH=rp01588en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.neulet.2003.12.117en_HK
dc.identifier.pmid15135890-
dc.identifier.scopuseid_2-s2.0-2342634487en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-2342634487&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume361en_HK
dc.identifier.issue1-3en_HK
dc.identifier.spage47en_HK
dc.identifier.epage51en_HK
dc.identifier.isiWOS:000221566100014-
dc.publisher.placeIrelanden_HK
dc.identifier.scopusauthoridCheung, ZH=6507483375en_HK
dc.identifier.scopusauthoridIp, NY=7005756760en_HK
dc.identifier.citeulike276922-

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