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Conference Paper: Lack of early activation of endoplasmic reticulum stress in beta-amyloid neurotoxicity

TitleLack of early activation of endoplasmic reticulum stress in beta-amyloid neurotoxicity
Authors
KeywordsAlzheimer’s disease
amyloid
ER stress
neurotoxicity
PERK
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. 52 Abstract no. P21-16 How to Cite?
AbstractBeta-amyloid (Ab) peptide neurotoxicity plays significant roles in Alzhei-mer’s disease (AD). Mutation of presenilin-1 (PS-1) gene sensitizes neuronsto Ab toxicity, also, causes dysfunctions of endoplasmic reticulum (ER).Therefore, ER stress receives increasing attention to AD. This study aimed toinvestigate different signaling pathways for ER stress responses in Abneurotoxicity. Rat cortical neurons exposed to Ab peptide did not showedinduction of alternative splicing in Xbp-1 mRNA by IRE-1, up-regulation of Xbp-1 mRNA by ATF-6 and PERK phosphorylation. After 16-h treatment ofAb peptide, there were induction of GRP 78 and GADD153 as well asactivation of caspase-12 and -7. These data suggested that ER stress is not anearly event involved in Ab neurotoxicity. Activation of JNK andphosphorylation of eIF2a were found at early time-point, however, thesesignaling events and neuronal cell death were not mediated by ER stressresponses. Taken together, ER stress seems to be a late response in Abpeptide-induced toxicity.
Persistent Identifierhttp://hdl.handle.net/10722/95717
ISSN
2015 Impact Factor: 3.842
2015 SCImago Journal Rankings: 2.021

 

DC FieldValueLanguage
dc.contributor.authorYu, MSen_HK
dc.contributor.authorSuen, KCen_HK
dc.contributor.authorKwok, NSen_HK
dc.contributor.authorSo, KFen_HK
dc.contributor.authorChang, RCCen_HK
dc.date.accessioned2010-09-25T16:11:03Z-
dc.date.available2010-09-25T16:11:03Z-
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. 52 Abstract no. P21-16en_HK
dc.identifier.issn0022-3042en_HK
dc.identifier.urihttp://hdl.handle.net/10722/95717-
dc.description.abstractBeta-amyloid (Ab) peptide neurotoxicity plays significant roles in Alzhei-mer’s disease (AD). Mutation of presenilin-1 (PS-1) gene sensitizes neuronsto Ab toxicity, also, causes dysfunctions of endoplasmic reticulum (ER).Therefore, ER stress receives increasing attention to AD. This study aimed toinvestigate different signaling pathways for ER stress responses in Abneurotoxicity. Rat cortical neurons exposed to Ab peptide did not showedinduction of alternative splicing in Xbp-1 mRNA by IRE-1, up-regulation of Xbp-1 mRNA by ATF-6 and PERK phosphorylation. After 16-h treatment ofAb peptide, there were induction of GRP 78 and GADD153 as well asactivation of caspase-12 and -7. These data suggested that ER stress is not anearly event involved in Ab neurotoxicity. Activation of JNK andphosphorylation of eIF2a were found at early time-point, however, thesesignaling events and neuronal cell death were not mediated by ER stressresponses. Taken together, ER stress seems to be a late response in Abpeptide-induced toxicity.-
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 disease-
dc.subjectamyloid-
dc.subjectER stress-
dc.subjectneurotoxicity-
dc.subjectPERK-
dc.titleLack of early activation of endoplasmic reticulum stress in beta-amyloid neurotoxicityen_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-3042&volume=88 Suppl. 1&spage=52 No. P21&epage=16&date=2004&atitle=Lack+of+early+activation+of+endoplasmic+reticulum+stress+in+beta-amyloid+neurotoxicityen_HK
dc.identifier.emailYu, MS: ymsmabel@graduate.hku.hken_HK
dc.identifier.emailSo, KF: hrmaskf@hkucc.hku.hken_HK
dc.identifier.emailChang, RCC: rccchang@hkucc.hku.hken_HK
dc.identifier.authoritySo, KF=rp00329en_HK
dc.identifier.authorityChang, RCC=rp00470en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1046/j.1474-1644.2003.2314p21_01.x-
dc.identifier.hkuros85903en_HK
dc.identifier.volume88en_HK
dc.identifier.spage52en_HK
dc.identifier.epage52en_HK

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