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Article: Severe acute respiratory syndrome coronavirus M protein inhibits type I interferon production by impeding theformation of TRAF3·TANK·TBK1/IKKε complex

TitleSevere acute respiratory syndrome coronavirus M protein inhibits type I interferon production by impeding theformation of TRAF3·TANK·TBK1/IKKε complex
Authors
Issue Date2009
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, 2009, v. 284 n. 24, p. 16202-16209 How to Cite?
AbstractSevere acute respiratory syndrome (SARS) coronavirus is highly pathogenic in humans and evades innate immunity at multiple levels. It has evolved various strategies to counteract the production and action of type I interferons, which mobilize the front-line defense against viral infection. In this study we demonstrate that SARS coronavirus M protein inhibits gene transcription of type I interferons. M protein potently antagonizes the activation of interferon-stimulated response element-dependent transcription by double-stranded RNA, RIG-I, MDA5, TBK1, IKKε, and virus-induced signaling adaptor (VISA) but has no influence on the transcriptional activity of this element when IRF3 or IRF7 is overexpressed. M protein physically associates with RIG-I, TBK1, IKKε, and TRAF3 and likely sequesters some of them in membrane-associated cytoplasmic compartments. Consequently, the expression of M protein prevents the formation of TRAF3-TANK-TBK1/ IKKε complex and thereby inhibits TBK1/IKKε-dependent activation of IRF3/IRF7 transcription factors. Taken together, our findings reveal a new mechanism by which SARS coronavirus circumvents the production of type I interferons. © 2009 by The American Society for Biochemistry and Molecular Biology, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/58265
ISSN
2015 Impact Factor: 4.258
2015 SCImago Journal Rankings: 3.151
PubMed Central ID
ISI Accession Number ID
Funding AgencyGrant Number
Research Fund for the Control of Infectious Disease04050052
Research Council of Hong Kong Food and Health Bureau
Funding Information:

This work was supported by the Research Fund for the Control of Infectious Disease (Project 04050052) from the Research Council of Hong Kong Food and Health Bureau.

References
Grants

 

DC FieldValueLanguage
dc.contributor.authorSiu, KLen_HK
dc.contributor.authorKok, KHen_HK
dc.contributor.authorNg, MHJen_HK
dc.contributor.authorPoon, VKMen_HK
dc.contributor.authorYuen, KYen_HK
dc.contributor.authorZheng, BJen_HK
dc.contributor.authorJin, DYen_HK
dc.date.accessioned2010-05-31T03:27:04Z-
dc.date.available2010-05-31T03:27:04Z-
dc.date.issued2009en_HK
dc.identifier.citationJournal Of Biological Chemistry, 2009, v. 284 n. 24, p. 16202-16209en_HK
dc.identifier.issn0021-9258en_HK
dc.identifier.urihttp://hdl.handle.net/10722/58265-
dc.description.abstractSevere acute respiratory syndrome (SARS) coronavirus is highly pathogenic in humans and evades innate immunity at multiple levels. It has evolved various strategies to counteract the production and action of type I interferons, which mobilize the front-line defense against viral infection. In this study we demonstrate that SARS coronavirus M protein inhibits gene transcription of type I interferons. M protein potently antagonizes the activation of interferon-stimulated response element-dependent transcription by double-stranded RNA, RIG-I, MDA5, TBK1, IKKε, and virus-induced signaling adaptor (VISA) but has no influence on the transcriptional activity of this element when IRF3 or IRF7 is overexpressed. M protein physically associates with RIG-I, TBK1, IKKε, and TRAF3 and likely sequesters some of them in membrane-associated cytoplasmic compartments. Consequently, the expression of M protein prevents the formation of TRAF3-TANK-TBK1/ IKKε complex and thereby inhibits TBK1/IKKε-dependent activation of IRF3/IRF7 transcription factors. Taken together, our findings reveal a new mechanism by which SARS coronavirus circumvents the production of type I interferons. © 2009 by The American Society for Biochemistry and Molecular Biology, Inc.en_HK
dc.languageengen_HK
dc.publisherAmerican Society for Biochemistry and Molecular Biology, Inc. The Journal's web site is located at http://www.jbc.org/en_HK
dc.relation.ispartofJournal of Biological Chemistryen_HK
dc.subject.meshAdaptor Proteins, Signal Transducing - metabolism-
dc.subject.meshInterferon Type I - genetics - immunology-
dc.subject.meshSARS Virus - immunology-
dc.subject.meshSevere Acute Respiratory Syndrome - immunology - virology-
dc.subject.meshViral Matrix Proteins - immunology - metabolism-
dc.titleSevere acute respiratory syndrome coronavirus M protein inhibits type I interferon production by impeding theformation of TRAF3·TANK·TBK1/IKKε complexen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0021-9258&volume=284&issue=24&spage=16202&epage=16209&date=2009&atitle=Severe+acute+respiratory+syndrome+coronavirus+M+protein+inhibits+type+I+interferon+production+by+impeding+the+formation+of+TRAF3.TANK.TBK1/IKKepsilon+complexen_HK
dc.identifier.emailKok, KH:khkok@hku.hken_HK
dc.identifier.emailYuen, KY:kyyuen@hkucc.hku.hken_HK
dc.identifier.emailZheng, BJ:bzheng@hkucc.hku.hken_HK
dc.identifier.emailJin, DY:dyjin@hkucc.hku.hken_HK
dc.identifier.authorityKok, KH=rp01455en_HK
dc.identifier.authorityYuen, KY=rp00366en_HK
dc.identifier.authorityZheng, BJ=rp00353en_HK
dc.identifier.authorityJin, DY=rp00452en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1074/jbc.M109.008227en_HK
dc.identifier.pmid19380580-
dc.identifier.pmcidPMC2713514-
dc.identifier.scopuseid_2-s2.0-67650230347en_HK
dc.identifier.hkuros166480en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-67650230347&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume284en_HK
dc.identifier.issue24en_HK
dc.identifier.spage16202en_HK
dc.identifier.epage16209en_HK
dc.identifier.isiWOS:000266730900017-
dc.publisher.placeUnited Statesen_HK
dc.relation.projectGene regulatory function and cellular partners of SARS-associated coronavirus nucleocapsid protein-
dc.identifier.scopusauthoridSiu, KL=7102312040en_HK
dc.identifier.scopusauthoridKok, KH=7006862631en_HK
dc.identifier.scopusauthoridNg, MHJ=27067825500en_HK
dc.identifier.scopusauthoridPoon, VKM=6603703384en_HK
dc.identifier.scopusauthoridYuen, KY=36078079100en_HK
dc.identifier.scopusauthoridZheng, BJ=7201780588en_HK
dc.identifier.scopusauthoridJin, DY=7201973614en_HK
dc.identifier.citeulike8143094-

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