File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Conference Paper: Molecular signaling of double-stranded RNA-dependent protein kinase (PKR) in beta-amyloid peptide (A beta)-induced neuronal death

TitleMolecular signaling of double-stranded RNA-dependent protein kinase (PKR) in beta-amyloid peptide (A beta)-induced neuronal death
Authors
KeywordsAlzheimer’s neurodegenerative diseases
signal transduction
neuronalapoptosis
beta-amyloid peptide
PKR
Issue Date2004
PublisherWiley-Blackwell Publishing Ltd.
Citation
The 6th Biennial Meeting of the Asian-Pacific Society for Neurochemistry, Hong Kong, 4-7 February 2004. In Journal of Neurochemistry, 2004, v. 88 n. S1, p. 20 Abstract no. C7-4 How to Cite?
AbstractAccumulation of Ab peptides has been considered to play important roles in thepathogenesis of Alzheimer’s disease (AD). Ab neurotoxicity is mediated via awide array of intracellular signaling pathways including increases in intracellularcalcium, different mitogen activated kinases and caspases. We have recentlyshown that attenuation of intracellular calcium provides significant but partialneuroprotective effect only. While endoplasmic reticulum (ER) stress responsesare not early activated right after exposure to Ab, phosphorylation of eukaryoticinitiation factor 2a (eIF2a) are detected at early time points. The roles of PKR arethus intensively studied from our group. We are the first laboratory to show theinvolvement of PKR in Ab neurotoxicity. PKR not just involves but playssignificant roles in Ab neurotoxicity. Over-expression of negatively mutatedneuroblastoma cells as well as primary cultured neurons from PKR knockout micedemonstrate a marked reduction of neuronal death. Postmortem AD brain sectionsalso elicit high immunoreactivity for phosphorylated PKR and eIF2a. We haverecently shown the upstream pathways for PKR to be activated by Ab. Early andmild activation of caspase-3 can function as signaling molecule mediatingactivation of PKR. Taken together, while PKR is not specific for Ab neurotoxicityand for AD, it will trigger pro-apoptotic signaling cascade in neurons once it isactivated. PKR may become a new potential pharmaceutical target for developingneuroprotective agent.
Persistent Identifierhttp://hdl.handle.net/10722/95614
ISSN
2015 Impact Factor: 3.842
2015 SCImago Journal Rankings: 2.021

 

DC FieldValueLanguage
dc.contributor.authorChang, RCCen_HK
dc.contributor.authorSuen, KCen_HK
dc.contributor.authorYu, MSen_HK
dc.contributor.authorLin, KFen_HK
dc.contributor.authorHugon, Jen_HK
dc.date.accessioned2010-09-25T16:07:48Z-
dc.date.available2010-09-25T16:07:48Z-
dc.date.issued2004en_HK
dc.identifier.citationThe 6th Biennial Meeting of the Asian-Pacific Society for Neurochemistry, Hong Kong, 4-7 February 2004. In Journal of Neurochemistry, 2004, v. 88 n. S1, p. 20 Abstract no. C7-4en_HK
dc.identifier.issn0022-3042en_HK
dc.identifier.urihttp://hdl.handle.net/10722/95614-
dc.description.abstractAccumulation of Ab peptides has been considered to play important roles in thepathogenesis of Alzheimer’s disease (AD). Ab neurotoxicity is mediated via awide array of intracellular signaling pathways including increases in intracellularcalcium, different mitogen activated kinases and caspases. We have recentlyshown that attenuation of intracellular calcium provides significant but partialneuroprotective effect only. While endoplasmic reticulum (ER) stress responsesare not early activated right after exposure to Ab, phosphorylation of eukaryoticinitiation factor 2a (eIF2a) are detected at early time points. The roles of PKR arethus intensively studied from our group. We are the first laboratory to show theinvolvement of PKR in Ab neurotoxicity. PKR not just involves but playssignificant roles in Ab neurotoxicity. Over-expression of negatively mutatedneuroblastoma cells as well as primary cultured neurons from PKR knockout micedemonstrate a marked reduction of neuronal death. Postmortem AD brain sectionsalso elicit high immunoreactivity for phosphorylated PKR and eIF2a. We haverecently shown the upstream pathways for PKR to be activated by Ab. Early andmild activation of caspase-3 can function as signaling molecule mediatingactivation of PKR. Taken together, while PKR is not specific for Ab neurotoxicityand for AD, it will trigger pro-apoptotic signaling cascade in neurons once it isactivated. PKR may become a new potential pharmaceutical target for developingneuroprotective agent.-
dc.languageengen_HK
dc.publisherWiley-Blackwell Publishing Ltd.en_HK
dc.relation.ispartofJournal of Neurochemistryen_HK
dc.rightsJournal of Neurochemistry. Copyright © Blackwell Publishing Ltd.en_HK
dc.subjectAlzheimer’s neurodegenerative diseases-
dc.subjectsignal transduction-
dc.subjectneuronalapoptosis-
dc.subjectbeta-amyloid peptide-
dc.subjectPKR-
dc.titleMolecular signaling of double-stranded RNA-dependent protein kinase (PKR) in beta-amyloid peptide (A beta)-induced neuronal deathen_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-3042&volume=88 Suppl. 1&spage=20 No. C7&epage=4&date=2004&atitle=Molecular+signaling+of+double-stranded+RNA-dependent+protein+kinase+(PKR)+in+beta-amyloid+peptide+(Ab)-induced+neuronal+deathen_HK
dc.identifier.emailChang, RCC: rccchang@hkucc.hku.hken_HK
dc.identifier.emailYu, MS: ymsmabel@graduate.hku.hken_HK
dc.identifier.emailHugon, J: jhugon@hkucc.hku.hken_HK
dc.identifier.authorityChang, RCC=rp00470en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1046/j..2003.0c7-1.x-
dc.identifier.hkuros85904en_HK
dc.identifier.volume88en_HK
dc.identifier.spage20en_HK
dc.identifier.epage20en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats