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Article: Proteomic analysis of neonatal mouse brain: Evidence for hypoxia- and ischemia-induced dephosphorylation of collapsin response mediator proteins
Title | Proteomic analysis of neonatal mouse brain: Evidence for hypoxia- and ischemia-induced dephosphorylation of collapsin response mediator proteins |
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Authors | |
Keywords | Collapsin response mediator proteins Cyclin-dependent kinase 5 Hypoxia and ischemia Hypoxia-ischemia-induced brain damage P35 |
Issue Date | 2008 |
Publisher | American 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? |
Abstract | Perinatal 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 Identifier | http://hdl.handle.net/10722/79949 |
ISSN | 2023 Impact Factor: 3.8 2023 SCImago Journal Rankings: 1.299 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Zhou, Y | en_HK |
dc.contributor.author | Bhatia, I | en_HK |
dc.contributor.author | Cai, Z | en_HK |
dc.contributor.author | He, QY | en_HK |
dc.contributor.author | Cheung, PT | en_HK |
dc.contributor.author | Chiu, JF | en_HK |
dc.date.accessioned | 2010-09-06T08:00:38Z | - |
dc.date.available | 2010-09-06T08:00:38Z | - |
dc.date.issued | 2008 | en_HK |
dc.identifier.citation | Journal Of Proteome Research, 2008, v. 7 n. 6, p. 2507-2515 | en_HK |
dc.identifier.issn | 1535-3893 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/79949 | - |
dc.description.abstract | Perinatal 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.language | eng | en_HK |
dc.publisher | American Chemical Society. The Journal's web site is located at http://pubs.acs.org/journals/jprobs | en_HK |
dc.relation.ispartof | Journal of Proteome Research | en_HK |
dc.subject | Collapsin response mediator proteins | en_HK |
dc.subject | Cyclin-dependent kinase 5 | en_HK |
dc.subject | Hypoxia and ischemia | en_HK |
dc.subject | Hypoxia-ischemia-induced brain damage | en_HK |
dc.subject | P35 | en_HK |
dc.title | Proteomic analysis of neonatal mouse brain: Evidence for hypoxia- and ischemia-induced dephosphorylation of collapsin response mediator proteins | en_HK |
dc.type | Article | en_HK |
dc.identifier.openurl | http://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+proteins | en_HK |
dc.identifier.email | Cheung, PT:ptcheung@hkucc.hku.hk | en_HK |
dc.identifier.authority | Cheung, PT=rp00351 | en_HK |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1021/pr800108k | en_HK |
dc.identifier.scopus | eid_2-s2.0-49849096759 | en_HK |
dc.identifier.hkuros | 151262 | en_HK |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-49849096759&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 7 | en_HK |
dc.identifier.issue | 6 | en_HK |
dc.identifier.spage | 2507 | en_HK |
dc.identifier.epage | 2515 | en_HK |
dc.identifier.isi | WOS:000256599000033 | - |
dc.publisher.place | United States | en_HK |
dc.identifier.scopusauthorid | Zhou, Y=7405366890 | en_HK |
dc.identifier.scopusauthorid | Bhatia, I=24597420400 | en_HK |
dc.identifier.scopusauthorid | Cai, Z=36604125100 | en_HK |
dc.identifier.scopusauthorid | He, QY=34770287900 | en_HK |
dc.identifier.scopusauthorid | Cheung, PT=7202595465 | en_HK |
dc.identifier.scopusauthorid | Chiu, JF=7201501692 | en_HK |
dc.identifier.issnl | 1535-3893 | - |