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Article: Severe acute respiratory syndrome-associated coronavirus nucleocapsid protein interacts with Smad3 and modulates transforming growth factor-β signaling

TitleSevere acute respiratory syndrome-associated coronavirus nucleocapsid protein interacts with Smad3 and modulates transforming growth factor-β signaling
Authors
Issue Date2008
PublisherAmerican Society for Biochemistry and Molecular Biology, Inc. The Journal's web site is located at http://www.jbc.org/
Citation
Journal Of Biological Chemistry, 2008, v. 283 n. 6, p. 3272-3280 How to Cite?
AbstractSevere acute respiratory syndrome (SARS) is an acute infectious disease with significant mortality. A typical clinical feature associated with SARS is pulmonary fibrosis and the associated lung failure. However, the underlying mechanism remains elusive. In this study, we demonstrate that SARS-associated coronavirus (SARS-CoV) nucleocapsid (N) protein potentiates transforming growth factor-β (TGF-β)-induced expression of plasminogen activator inhibitor-1 but attenuates Smad3/Smad4-mediated apoptosis of human peripheral lung epithelial HPL1 cells. The promoting effect of N protein on the transcriptional responses of TGF-β is Smad3-specific. N protein associates with Smad3 and promotes Smad3-p300 complex formation while it interferes with the complex formation between Smad3 and Smad4. These findings provide evidence of a novel mechanism whereby N protein modulates TGF-β signaling to block apoptosis of SARS-CoV-infected host cells and meanwhile promote tissue fibrosis. Our results reveal a novel mode of Smad3 action in a Smad4-independent manner and may lead to successful strategies for SARS treatment by targeting the TGF-β signaling molecules. © 2008 by The American Society for Biochemistry and Molecular Biology, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/148549
ISSN
2015 Impact Factor: 4.258
2015 SCImago Journal Rankings: 3.151
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorZhao, Xen_US
dc.contributor.authorNicholls, JMen_US
dc.contributor.authorChen, YGen_US
dc.date.accessioned2012-05-29T06:13:39Z-
dc.date.available2012-05-29T06:13:39Z-
dc.date.issued2008en_US
dc.identifier.citationJournal Of Biological Chemistry, 2008, v. 283 n. 6, p. 3272-3280en_US
dc.identifier.issn0021-9258en_US
dc.identifier.urihttp://hdl.handle.net/10722/148549-
dc.description.abstractSevere acute respiratory syndrome (SARS) is an acute infectious disease with significant mortality. A typical clinical feature associated with SARS is pulmonary fibrosis and the associated lung failure. However, the underlying mechanism remains elusive. In this study, we demonstrate that SARS-associated coronavirus (SARS-CoV) nucleocapsid (N) protein potentiates transforming growth factor-β (TGF-β)-induced expression of plasminogen activator inhibitor-1 but attenuates Smad3/Smad4-mediated apoptosis of human peripheral lung epithelial HPL1 cells. The promoting effect of N protein on the transcriptional responses of TGF-β is Smad3-specific. N protein associates with Smad3 and promotes Smad3-p300 complex formation while it interferes with the complex formation between Smad3 and Smad4. These findings provide evidence of a novel mechanism whereby N protein modulates TGF-β signaling to block apoptosis of SARS-CoV-infected host cells and meanwhile promote tissue fibrosis. Our results reveal a novel mode of Smad3 action in a Smad4-independent manner and may lead to successful strategies for SARS treatment by targeting the TGF-β signaling molecules. © 2008 by The American Society for Biochemistry and Molecular Biology, Inc.en_US
dc.languageengen_US
dc.publisherAmerican Society for Biochemistry and Molecular Biology, Inc. The Journal's web site is located at http://www.jbc.org/en_US
dc.relation.ispartofJournal of Biological Chemistryen_US
dc.rightsJournal of Biological Chemistry. Copyright © American Society for Biochemistry and Molecular Biology, Inc.-
dc.subject.meshAnimalsen_US
dc.subject.meshApoptosisen_US
dc.subject.meshCell Lineen_US
dc.subject.meshFibrosis - Pathologyen_US
dc.subject.meshGene Expression Regulation, Viralen_US
dc.subject.meshHumansen_US
dc.subject.meshMiceen_US
dc.subject.meshNucleocapsid Proteins - Metabolismen_US
dc.subject.meshProtein Bindingen_US
dc.subject.meshProtein Structure, Tertiaryen_US
dc.subject.meshSars Virus - Metabolismen_US
dc.subject.meshSignal Transductionen_US
dc.subject.meshSmad3 Protein - Metabolismen_US
dc.subject.meshSmad4 Protein - Metabolismen_US
dc.subject.meshTransforming Growth Factor Beta - Metabolismen_US
dc.titleSevere acute respiratory syndrome-associated coronavirus nucleocapsid protein interacts with Smad3 and modulates transforming growth factor-β signalingen_US
dc.typeArticleen_US
dc.identifier.emailNicholls, JM:nicholls@pathology.hku.hken_US
dc.identifier.authorityNicholls, JM=rp00364en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1074/jbc.M708033200en_US
dc.identifier.pmid18055455-
dc.identifier.scopuseid_2-s2.0-41249096923en_US
dc.identifier.hkuros147216-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-41249096923&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume283en_US
dc.identifier.issue6en_US
dc.identifier.spage3272en_US
dc.identifier.epage3280en_US
dc.identifier.isiWOS:000253083000031-
dc.publisher.placeUnited Statesen_US

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