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Article: Beta-amyloid peptides induces neuronal apoptosis via a mechanism independent of unfolded protein responses

TitleBeta-amyloid peptides induces neuronal apoptosis via a mechanism independent of unfolded protein responses
Authors
Issue Date2006
PublisherSpringer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=1360-8185
Citation
Apoptosis, 2006, v. 11 n. 5, p. 687-700 How to Cite?
AbstractAccumulation of beta-amyloid (Aβ) peptides in senile plaques is one of the pathological hallmarks in Alzheimer's disease (AD), which can trigger apoptosis. We have previously demonstrated that Aβ triggered calcium release from the ER. Depletion of ER Ca2+ ions has been reported leading to unfolded protein responses (UPR). While hypothesis has been made about UPR and neurodegeneration in AD, little is known about the effects of extracellular accumulation of Aβ on UPR. We have shown previously that activation of PKR in Aβ-triggered apoptosis. Since UPR can trigger PKR, our study aims to elucidate whether extracellular accumulation of Aβ peptides induce UPR in cultured neurons. Our results showed that Aβ could not trigger UPR signalings including phosphorylation of PERK, alternative cleavage of xbp-1 mRNA and induction of transcription of xbp-1 and Gadd153. Taken together, our results suggest that extracellular accumulation of Aβ peptides induce apoptosis via a mechanism independent of UPR. © 2006 Springer Science + Business Media, LLC.
Persistent Identifierhttp://hdl.handle.net/10722/67973
ISSN
2015 Impact Factor: 3.592
2015 SCImago Journal Rankings: 1.554
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYu, MSen_HK
dc.contributor.authorSuen, KCen_HK
dc.contributor.authorKwok, NSen_HK
dc.contributor.authorSo, KFen_HK
dc.contributor.authorHugon, Jen_HK
dc.contributor.authorChuenChung Chang, Ren_HK
dc.date.accessioned2010-09-06T05:59:57Z-
dc.date.available2010-09-06T05:59:57Z-
dc.date.issued2006en_HK
dc.identifier.citationApoptosis, 2006, v. 11 n. 5, p. 687-700en_HK
dc.identifier.issn1360-8185en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67973-
dc.description.abstractAccumulation of beta-amyloid (Aβ) peptides in senile plaques is one of the pathological hallmarks in Alzheimer's disease (AD), which can trigger apoptosis. We have previously demonstrated that Aβ triggered calcium release from the ER. Depletion of ER Ca2+ ions has been reported leading to unfolded protein responses (UPR). While hypothesis has been made about UPR and neurodegeneration in AD, little is known about the effects of extracellular accumulation of Aβ on UPR. We have shown previously that activation of PKR in Aβ-triggered apoptosis. Since UPR can trigger PKR, our study aims to elucidate whether extracellular accumulation of Aβ peptides induce UPR in cultured neurons. Our results showed that Aβ could not trigger UPR signalings including phosphorylation of PERK, alternative cleavage of xbp-1 mRNA and induction of transcription of xbp-1 and Gadd153. Taken together, our results suggest that extracellular accumulation of Aβ peptides induce apoptosis via a mechanism independent of UPR. © 2006 Springer Science + Business Media, LLC.en_HK
dc.languageengen_HK
dc.publisherSpringer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=1360-8185en_HK
dc.relation.ispartofApoptosisen_HK
dc.subject.meshAmyloid beta-Peptides - chemistry - pharmacologyen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshApoptosis - drug effectsen_HK
dc.subject.meshBasic-Leucine Zipper Transcription Factors - metabolismen_HK
dc.subject.meshCell Culture Techniquesen_HK
dc.subject.meshCells, Cultureden_HK
dc.subject.meshCerebral Cortex - cytology - embryologyen_HK
dc.subject.meshDNA-Binding Proteinsen_HK
dc.subject.meshNeoplasm Proteins - metabolismen_HK
dc.subject.meshNeurons - cytology - drug effects - physiologyen_HK
dc.subject.meshPeptide Fragments - pharmacologyen_HK
dc.subject.meshProtein Denaturation - physiologyen_HK
dc.subject.meshRNA, Messenger - metabolismen_HK
dc.subject.meshRatsen_HK
dc.subject.meshRats, Sprague-Dawleyen_HK
dc.subject.meshTime Factorsen_HK
dc.subject.meshTranscription Factorsen_HK
dc.titleBeta-amyloid peptides induces neuronal apoptosis via a mechanism independent of unfolded protein responsesen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1360-8185&volume=11&spage=687&epage=700&date=2006&atitle=Beta-amyloid+peptides+induces+neuronal+apoptosis+via+a+mechanism+independent+of+unfolded+protein+responsesen_HK
dc.identifier.emailSo, KF:hrmaskf@hkucc.hku.hken_HK
dc.identifier.emailChuenChung Chang, R:rccchang@hkucc.hku.hken_HK
dc.identifier.authoritySo, KF=rp00329en_HK
dc.identifier.authorityChuenChung Chang, R=rp00470en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1007/s10495-006-5540-1en_HK
dc.identifier.pmid16532272-
dc.identifier.scopuseid_2-s2.0-33745019916en_HK
dc.identifier.hkuros148334en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33745019916&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume11en_HK
dc.identifier.issue5en_HK
dc.identifier.spage687en_HK
dc.identifier.epage700en_HK
dc.identifier.isiWOS:000238154000004-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridYu, MS=35346047600en_HK
dc.identifier.scopusauthoridSuen, KC=7004577222en_HK
dc.identifier.scopusauthoridKwok, NS=24341390000en_HK
dc.identifier.scopusauthoridSo, KF=34668391300en_HK
dc.identifier.scopusauthoridHugon, J=7103202992en_HK
dc.identifier.scopusauthoridChuenChung Chang, R=7403713410en_HK

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