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Article: In vivo cellular adaptation to ER stress: Survival strategies with double-edged consequences

TitleIn vivo cellular adaptation to ER stress: Survival strategies with double-edged consequences
Authors
KeywordsCell fate
Development
Disorders
ER stress
Unfolded protein response
Issue Date2010
PublisherThe Company of Biologists Ltd.
Citation
Journal Of Cell Science, 2010, v. 123 n. 13, p. 2145-2154 How to Cite?
AbstractDisturbances to the balance of protein synthesis, folding and secretion in the endoplasmic reticulum (ER) induce stress and thereby the ER stress signaling (ERSS) response, which alleviates this stress. In this Commentary, we review the emerging idea that ER stress caused by abnormal physiological conditions and/or mutations in genes that encode client proteins of the ER is a key factor underlying different developmental processes and the pathology of diverse diseases, including diabetes, neurodegeneration and skeletal dysplasias. Recent studies in mouse models indicate that the effect of ERSS in vivo and the nature of the cellular strategies induced to ameliorate pathological ER stress are crucial factors in determining cell fate and clinical disease features. Importantly, ERSS can affect cellular proliferation and the differentiation program; cells that survive the stress can become 'reprogrammed' or dysfunctional. These cell-autonomous adaptation strategies can generate a spectrum of context-dependent cellular consequences, ranging from recovery to death. Secondary effects can include altered cell-extracellular-matrix interactions and non-cell-autonomous alteration of paracrine signaling, which contribute to the final phenotypic outcome. Recent reports showing that ER stress can be alleviated by chemical compounds suggest the potential for novel therapeutic approaches. © 2010. Published by The Company of Biologists Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/129098
ISSN
2015 Impact Factor: 4.706
2015 SCImago Journal Rankings: 3.501
ISI Accession Number ID
Funding AgencyGrant Number
University Grants Committee of Hong KongAoE/M-04/04
National Health and Medical Research Council of Australia
Funding Information:

The authors are supported by the University Grants Committee of Hong Kong Area of Excellence programme AoE/M-04/04, and the National Health and Medical Research Council of Australia (J.F.B.).

References
Grants

 

DC FieldValueLanguage
dc.contributor.authorTsang, KYen_HK
dc.contributor.authorChan, Den_HK
dc.contributor.authorBateman, JFen_HK
dc.contributor.authorCheah, KSEen_HK
dc.date.accessioned2010-12-23T08:32:28Z-
dc.date.available2010-12-23T08:32:28Z-
dc.date.issued2010en_HK
dc.identifier.citationJournal Of Cell Science, 2010, v. 123 n. 13, p. 2145-2154en_HK
dc.identifier.issn0021-9533en_HK
dc.identifier.urihttp://hdl.handle.net/10722/129098-
dc.description.abstractDisturbances to the balance of protein synthesis, folding and secretion in the endoplasmic reticulum (ER) induce stress and thereby the ER stress signaling (ERSS) response, which alleviates this stress. In this Commentary, we review the emerging idea that ER stress caused by abnormal physiological conditions and/or mutations in genes that encode client proteins of the ER is a key factor underlying different developmental processes and the pathology of diverse diseases, including diabetes, neurodegeneration and skeletal dysplasias. Recent studies in mouse models indicate that the effect of ERSS in vivo and the nature of the cellular strategies induced to ameliorate pathological ER stress are crucial factors in determining cell fate and clinical disease features. Importantly, ERSS can affect cellular proliferation and the differentiation program; cells that survive the stress can become 'reprogrammed' or dysfunctional. These cell-autonomous adaptation strategies can generate a spectrum of context-dependent cellular consequences, ranging from recovery to death. Secondary effects can include altered cell-extracellular-matrix interactions and non-cell-autonomous alteration of paracrine signaling, which contribute to the final phenotypic outcome. Recent reports showing that ER stress can be alleviated by chemical compounds suggest the potential for novel therapeutic approaches. © 2010. Published by The Company of Biologists Ltd.en_HK
dc.languageengen_US
dc.publisherThe Company of Biologists Ltd.-
dc.relation.ispartofJournal of Cell Scienceen_HK
dc.subjectCell fateen_HK
dc.subjectDevelopmenten_HK
dc.subjectDisordersen_HK
dc.subjectER stressen_HK
dc.subjectUnfolded protein responseen_HK
dc.subject.meshAdaptation, Physiological-
dc.subject.meshAnimals-
dc.subject.meshCell Survival-
dc.subject.meshEndoplasmic Reticulum - physiology-
dc.subject.meshStress, Physiological-
dc.titleIn vivo cellular adaptation to ER stress: Survival strategies with double-edged consequencesen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0021-9533&volume=123&issue=Pt13&spage=2145&epage=2154&date=2010&atitle=In+vivo+cellular+adaptation+to+ER+stress:+survival+strategies+with+double-edged+consequences-
dc.identifier.emailChan, D:chand@hkucc.hku.hken_HK
dc.identifier.emailCheah, KSE:hrmbdkc@hku.hken_HK
dc.identifier.authorityChan, D=rp00540en_HK
dc.identifier.authorityCheah, KSE=rp00342en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1242/jcs.068833en_HK
dc.identifier.pmid20554893en_HK
dc.identifier.scopuseid_2-s2.0-77954354827en_HK
dc.identifier.hkuros178269en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77954354827&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume123en_HK
dc.identifier.issue13en_HK
dc.identifier.spage2145en_HK
dc.identifier.epage2154en_HK
dc.identifier.eissn1477-9137-
dc.identifier.isiWOS:000278856400001-
dc.publisher.placeUnited Kingdomen_HK
dc.relation.projectDevelopmental genomics and skeletal research-
dc.identifier.scopusauthoridTsang, KY=22635904200en_HK
dc.identifier.scopusauthoridChan, D=7402216545en_HK
dc.identifier.scopusauthoridBateman, JF=16135557700en_HK
dc.identifier.scopusauthoridCheah, KSE=35387746200en_HK

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