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Article: Proteomic analysis of neonatal mouse brain: Evidence for hypoxia- and ischemia-induced dephosphorylation of collapsin response mediator proteins

TitleProteomic analysis of neonatal mouse brain: Evidence for hypoxia- and ischemia-induced dephosphorylation of collapsin response mediator proteins
Authors
KeywordsCollapsin response mediator proteins
Cyclin-dependent kinase 5
Hypoxia and ischemia
Hypoxia-ischemia-induced brain damage
P35
Issue Date2008
PublisherAmerican Chemical Society. The Journal's web site is located at http://pubs.acs.org/journals/jprobs
Citation
Journal Of Proteome Research, 2008, v. 7 n. 6, p. 2507-2515 How to Cite?
AbstractPerinatal hypoxia and ischemia (HI) are a significant cause of mortality and morbidity. To understand the molecular mechanisms for Hl-induced brain damage, here we used a proteomic approach to analyze the alteration and modification of proteins in neonatal mouse brain 24 h after HI treatment. Significant changes of collapsin response mediator proteins (CRMPs) were observed in HI brain. CRMPs are a family of cytosolic proteins involved in axonal guidance and neuronal outgrowth. We found that CRMP2, CRMP4 and CRMP5 proteins were altered post-translationally after HI treatment. Mass spectrometric and Western blot analyses detected hypophosphorylated CRMP proteins after HI. Further analysis of CRMP kinases indicated inactivation of cyclin dependent kinase 5 (CDK5), a priming kinase of CRMPs and a neuronal specific kinase that plays pivotal roles in neuronal development and survival. The reduction of CDK5 activity was associated with underexpression of its activator p35. Taken together, our findings reveal Hl-induced dephosphorylation of CRMPs in neonatal brain and suggest a novel mechanism for this modification. Hypophosphorylated CRMPs might be implicated in the pathogenesis of Hl-related neurological disorders. © 2008 American Chemical Society.
Persistent Identifierhttp://hdl.handle.net/10722/79949
ISSN
2015 Impact Factor: 4.173
2015 SCImago Journal Rankings: 1.962
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorZhou, Yen_HK
dc.contributor.authorBhatia, Ien_HK
dc.contributor.authorCai, Zen_HK
dc.contributor.authorHe, QYen_HK
dc.contributor.authorCheung, PTen_HK
dc.contributor.authorChiu, JFen_HK
dc.date.accessioned2010-09-06T08:00:38Z-
dc.date.available2010-09-06T08:00:38Z-
dc.date.issued2008en_HK
dc.identifier.citationJournal Of Proteome Research, 2008, v. 7 n. 6, p. 2507-2515en_HK
dc.identifier.issn1535-3893en_HK
dc.identifier.urihttp://hdl.handle.net/10722/79949-
dc.description.abstractPerinatal hypoxia and ischemia (HI) are a significant cause of mortality and morbidity. To understand the molecular mechanisms for Hl-induced brain damage, here we used a proteomic approach to analyze the alteration and modification of proteins in neonatal mouse brain 24 h after HI treatment. Significant changes of collapsin response mediator proteins (CRMPs) were observed in HI brain. CRMPs are a family of cytosolic proteins involved in axonal guidance and neuronal outgrowth. We found that CRMP2, CRMP4 and CRMP5 proteins were altered post-translationally after HI treatment. Mass spectrometric and Western blot analyses detected hypophosphorylated CRMP proteins after HI. Further analysis of CRMP kinases indicated inactivation of cyclin dependent kinase 5 (CDK5), a priming kinase of CRMPs and a neuronal specific kinase that plays pivotal roles in neuronal development and survival. The reduction of CDK5 activity was associated with underexpression of its activator p35. Taken together, our findings reveal Hl-induced dephosphorylation of CRMPs in neonatal brain and suggest a novel mechanism for this modification. Hypophosphorylated CRMPs might be implicated in the pathogenesis of Hl-related neurological disorders. © 2008 American Chemical Society.en_HK
dc.languageengen_HK
dc.publisherAmerican Chemical Society. The Journal's web site is located at http://pubs.acs.org/journals/jprobsen_HK
dc.relation.ispartofJournal of Proteome Researchen_HK
dc.subjectCollapsin response mediator proteinsen_HK
dc.subjectCyclin-dependent kinase 5en_HK
dc.subjectHypoxia and ischemiaen_HK
dc.subjectHypoxia-ischemia-induced brain damageen_HK
dc.subjectP35en_HK
dc.titleProteomic analysis of neonatal mouse brain: Evidence for hypoxia- and ischemia-induced dephosphorylation of collapsin response mediator proteinsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1535-3893&volume=7&spage=2507&epage=&date=2008&atitle=Proteomic+analysis+of+neonatal+mouse+brain:+evidence+for+hypoxia-+and+ischemia-induced+dephosphorylation+of+collapsin+response+mediator+proteinsen_HK
dc.identifier.emailCheung, PT:ptcheung@hkucc.hku.hken_HK
dc.identifier.authorityCheung, PT=rp00351en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1021/pr800108ken_HK
dc.identifier.scopuseid_2-s2.0-49849096759en_HK
dc.identifier.hkuros151262en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-49849096759&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume7en_HK
dc.identifier.issue6en_HK
dc.identifier.spage2507en_HK
dc.identifier.epage2515en_HK
dc.identifier.isiWOS:000256599000033-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridZhou, Y=7405366890en_HK
dc.identifier.scopusauthoridBhatia, I=24597420400en_HK
dc.identifier.scopusauthoridCai, Z=36604125100en_HK
dc.identifier.scopusauthoridHe, QY=34770287900en_HK
dc.identifier.scopusauthoridCheung, PT=7202595465en_HK
dc.identifier.scopusauthoridChiu, JF=7201501692en_HK

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