Severe acute respiratory syndrome coronavirus papain-like protease suppressed alpha interferon-induced responses through downregulation of extracellular signal-regulated kinase 1-mediated signalling pathways
Identifieur interne : 002359 ( Main/Exploration ); précédent : 002358; suivant : 002360Severe acute respiratory syndrome coronavirus papain-like protease suppressed alpha interferon-induced responses through downregulation of extracellular signal-regulated kinase 1-mediated signalling pathways
Auteurs : Shih-Wein Li [Taïwan] ; Chien-Chen Lai [Taïwan] ; Jia-Fong Ping [Taïwan] ; Fuu-Jen Tsai [Taïwan] ; LEI WAN [Taïwan] ; Ying-Ju Lin [Taïwan] ; Szu-Hao Kung [Taïwan] ; Cheng-Wen Lin [Taïwan]Source :
- Journal of general virology [ 0022-1317 ] ; 2011.
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Abstract
Severe acute respiratory syndrome coronavirus (SARS-CoV) papain-like protease (PLpro), a deubiquitinating enzyme, reportedly blocks poly I:C-induced activation of interferon regulatory factor 3 and nuclear factor kappa B, reducing interferon (IFN) induction. This study investigated type I IFN antagonist mechanism of PLpro in human promonocytes. PLpro antagonized IFN-α-induced responses such as interferon-stimulated response element- and AP-1-driven promoter activation, protein kinase R, 2'-5'-oligoadenylate synthetase (OAS), interleukin (IL)-6 and IL-8 expression, and signal transducers and activators of transcription (STAT) 1 (Tyr701), STAT1 (Ser727) and c-Jun phosphorylation. A proteomics approach demonstrated downregulation of extracellular signal-regulated kinase (ERK) 1 and upregulation of ubiquitin-conjugating enzyme (UBC) E2-25k as inhibitory mechanism of PLpro on IFN-α-induced responses. IFN-α treatment significantly induced mRNA expression of UBC E2-25k, but not ERK1, causing time-dependent decrease of ERK1, but not ERK2, in PLpro-expressing cells. Poly-ubiquitination of ERK1 showed a relationship between ERK1 and ubiquitin proteasome signalling pathways associated with IFN antagonism by PLpro. Combination treatment of IFN-α and the proteasome inhibitor MG-132 showed a time-dependent restoration of ERK1 protein levels and significant increase of ERK1, STAT1 and c-Jun phosphorylation in PLpro-expressing cells. Importantly, PD098059 (an ERK1/2 inhibitor) treatment significantly reduced IFN-α-induced ERK1 and STAT1 phosphorylation, inhibiting IFN-α-induced expression of 2'-5'-OAS in vector control cells and PLpro-expressing cells. Overall results proved downregulation of ERK1 by ubiquitin proteasomes and suppression of interaction between ERK1 and STAT1 as type I IFN antagonist function of SARS-CoV PLpro.
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aut.</sZ></inist:fA14><country>Taïwan</country><wicri:noRegion>Wufeng, Taichung</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">11-0239193</idno><date when="2011">2011</date><idno type="stanalyst">PASCAL 11-0239193 INIST</idno><idno type="RBID">Pascal:11-0239193</idno><idno type="wicri:Area/PascalFrancis/Corpus">000110</idno><idno type="wicri:Area/PascalFrancis/Curation">000878</idno><idno type="wicri:Area/PascalFrancis/Checkpoint">000080</idno><idno type="wicri:explorRef" wicri:stream="PascalFrancis" wicri:step="Checkpoint">000080</idno><idno type="wicri:doubleKey">0022-1317:2011:Li S:severe:acute:respiratory</idno><idno type="wicri:Area/Main/Merge">002387</idno><idno type="wicri:Area/Main/Curation">002359</idno><idno type="wicri:Area/Main/Exploration">002359</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Severe acute respiratory syndrome coronavirus papain-like protease suppressed alpha interferon-induced responses through downregulation of extracellular signal-regulated kinase 1-mediated signalling pathways</title><author><name sortKey="Li, Shih Wein" sort="Li, Shih Wein" uniqKey="Li S" first="Shih-Wein" last="Li">Shih-Wein Li</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Medical Laboratory Science and Biotechnology, China Medical University</s1><s2>Taichung</s2><s3>TWN</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>8 aut.</sZ></inist:fA14><country>Taïwan</country><wicri:noRegion>Taichung</wicri:noRegion></affiliation><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Institute of Molecular Biology, National Chung Hsing University</s1><s2>Taichung</s2><s3>TWN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ></inist:fA14><country>Taïwan</country><wicri:noRegion>Taichung</wicri:noRegion></affiliation></author><author><name sortKey="Lai, Chien Chen" sort="Lai, Chien Chen" uniqKey="Lai C" first="Chien-Chen" last="Lai">Chien-Chen Lai</name><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Institute of Molecular Biology, National Chung Hsing University</s1><s2>Taichung</s2><s3>TWN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ></inist:fA14><country>Taïwan</country><wicri:noRegion>Taichung</wicri:noRegion></affiliation><affiliation wicri:level="1"><inist:fA14 i1="03"><s1>Department of Medical Genetics and Medical Research, China Medical University Hospital</s1><s2>Taichung</s2><s3>TWN</s3><sZ>2 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Taïwan</country><wicri:noRegion>Taichung</wicri:noRegion></affiliation></author><author><name sortKey="Ping, Jia Fong" sort="Ping, Jia Fong" uniqKey="Ping J" first="Jia-Fong" last="Ping">Jia-Fong Ping</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Medical Laboratory Science and Biotechnology, China Medical University</s1><s2>Taichung</s2><s3>TWN</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>8 aut.</sZ></inist:fA14><country>Taïwan</country><wicri:noRegion>Taichung</wicri:noRegion></affiliation></author><author><name sortKey="Tsai, Fuu Jen" sort="Tsai, Fuu Jen" uniqKey="Tsai F" first="Fuu-Jen" last="Tsai">Fuu-Jen Tsai</name><affiliation wicri:level="1"><inist:fA14 i1="03"><s1>Department of Medical Genetics and Medical Research, China Medical University Hospital</s1><s2>Taichung</s2><s3>TWN</s3><sZ>2 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Taïwan</country><wicri:noRegion>Taichung</wicri:noRegion></affiliation></author><author><name sortKey="Lei Wan" sort="Lei Wan" uniqKey="Lei Wan" last="Lei Wan">LEI WAN</name><affiliation wicri:level="1"><inist:fA14 i1="03"><s1>Department of Medical Genetics and Medical Research, China Medical University Hospital</s1><s2>Taichung</s2><s3>TWN</s3><sZ>2 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Taïwan</country><wicri:noRegion>Taichung</wicri:noRegion></affiliation></author><author><name sortKey="Lin, Ying Ju" sort="Lin, Ying Ju" uniqKey="Lin Y" first="Ying-Ju" last="Lin">Ying-Ju Lin</name><affiliation wicri:level="1"><inist:fA14 i1="03"><s1>Department of Medical Genetics and Medical Research, China Medical University Hospital</s1><s2>Taichung</s2><s3>TWN</s3><sZ>2 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Taïwan</country><wicri:noRegion>Taichung</wicri:noRegion></affiliation></author><author><name sortKey="Kung, Szu Hao" sort="Kung, Szu Hao" uniqKey="Kung S" first="Szu-Hao" last="Kung">Szu-Hao Kung</name><affiliation wicri:level="1"><inist:fA14 i1="04"><s1>Department of Biotechnology and Laboratory Science in Medicine, National Yang Ming University</s1><s2>Taipei</s2><s3>TWN</s3><sZ>7 aut.</sZ></inist:fA14><country>Taïwan</country><wicri:noRegion>Taipei</wicri:noRegion></affiliation></author><author><name sortKey="Lin, Cheng Wen" sort="Lin, Cheng Wen" uniqKey="Lin C" first="Cheng-Wen" last="Lin">Cheng-Wen Lin</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Medical Laboratory Science and Biotechnology, China Medical University</s1><s2>Taichung</s2><s3>TWN</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>8 aut.</sZ></inist:fA14><country>Taïwan</country><wicri:noRegion>Taichung</wicri:noRegion></affiliation><affiliation wicri:level="1"><inist:fA14 i1="05"><s1>Clinical Virology Laboratory, Department of Laboratory Medicine, China Medical University Hospital</s1><s2>Taichung</s2><s3>TWN</s3><sZ>8 aut.</sZ></inist:fA14><country>Taïwan</country><wicri:noRegion>Taichung</wicri:noRegion></affiliation><affiliation wicri:level="1"><inist:fA14 i1="06"><s1>Department of Biotechnology, Asia University</s1><s2>Wufeng, Taichung</s2><s3>TWN</s3><sZ>8 aut.</sZ></inist:fA14><country>Taïwan</country><wicri:noRegion>Wufeng, Taichung</wicri:noRegion></affiliation></author></analytic><series><title level="j" type="main">Journal of general virology</title><title level="j" type="abbreviated">J. gen. virol.</title><idno type="ISSN">0022-1317</idno><imprint><date when="2011">2011</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Journal of general virology</title><title level="j" type="abbreviated">J. gen. virol.</title><idno type="ISSN">0022-1317</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Alpha interferon</term><term>Coronavirus</term><term>Mitogen-activated protein kinase</term><term>Severe acute respiratory syndrome</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Coronavirus</term><term>Mitogen-activated protein kinase</term><term>Syndrome respiratoire aigu sévère</term><term>Interféron alpha</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Severe acute respiratory syndrome coronavirus (SARS-CoV) papain-like protease (PLpro), a deubiquitinating enzyme, reportedly blocks poly I:C-induced activation of interferon regulatory factor 3 and nuclear factor kappa B, reducing interferon (IFN) induction. This study investigated type I IFN antagonist mechanism of PLpro in human promonocytes. PLpro antagonized IFN-α-induced responses such as interferon-stimulated response element- and AP-1-driven promoter activation, protein kinase R, 2'-5'-oligoadenylate synthetase (OAS), interleukin (IL)-6 and IL-8 expression, and signal transducers and activators of transcription (STAT) 1 (Tyr701), STAT1 (Ser727) and c-Jun phosphorylation. A proteomics approach demonstrated downregulation of extracellular signal-regulated kinase (ERK) 1 and upregulation of ubiquitin-conjugating enzyme (UBC) E2-25k as inhibitory mechanism of PLpro on IFN-α-induced responses. IFN-α treatment significantly induced mRNA expression of UBC E2-25k, but not ERK1, causing time-dependent decrease of ERK1, but not ERK2, in PLpro-expressing cells. Poly-ubiquitination of ERK1 showed a relationship between ERK1 and ubiquitin proteasome signalling pathways associated with IFN antagonism by PLpro. Combination treatment of IFN-α and the proteasome inhibitor MG-132 showed a time-dependent restoration of ERK1 protein levels and significant increase of ERK1, STAT1 and c-Jun phosphorylation in PLpro-expressing cells. Importantly, PD098059 (an ERK1/2 inhibitor) treatment significantly reduced IFN-α-induced ERK1 and STAT1 phosphorylation, inhibiting IFN-α-induced expression of 2'-5'-OAS in vector control cells and PLpro-expressing cells. Overall results proved downregulation of ERK1 by ubiquitin proteasomes and suppression of interaction between ERK1 and STAT1 as type I IFN antagonist function of SARS-CoV PLpro.</div></front></TEI><affiliations><list><country><li>Taïwan</li></country></list><tree><country name="Taïwan"><noRegion><name sortKey="Li, Shih Wein" sort="Li, Shih Wein" uniqKey="Li S" first="Shih-Wein" last="Li">Shih-Wein Li</name></noRegion><name sortKey="Kung, Szu Hao" sort="Kung, Szu Hao" uniqKey="Kung S" first="Szu-Hao" last="Kung">Szu-Hao Kung</name><name sortKey="Lai, Chien Chen" sort="Lai, Chien Chen" uniqKey="Lai C" first="Chien-Chen" last="Lai">Chien-Chen Lai</name><name sortKey="Lai, Chien Chen" sort="Lai, Chien Chen" uniqKey="Lai C" first="Chien-Chen" last="Lai">Chien-Chen Lai</name><name sortKey="Lei Wan" sort="Lei Wan" uniqKey="Lei Wan" last="Lei Wan">LEI WAN</name><name sortKey="Li, Shih Wein" sort="Li, Shih Wein" uniqKey="Li S" first="Shih-Wein" last="Li">Shih-Wein Li</name><name sortKey="Lin, Cheng Wen" sort="Lin, Cheng Wen" uniqKey="Lin C" first="Cheng-Wen" last="Lin">Cheng-Wen Lin</name><name sortKey="Lin, Cheng Wen" sort="Lin, Cheng Wen" uniqKey="Lin C" first="Cheng-Wen" last="Lin">Cheng-Wen Lin</name><name sortKey="Lin, Cheng Wen" sort="Lin, Cheng Wen" uniqKey="Lin C" first="Cheng-Wen" last="Lin">Cheng-Wen Lin</name><name sortKey="Lin, Ying Ju" sort="Lin, Ying Ju" uniqKey="Lin Y" first="Ying-Ju" last="Lin">Ying-Ju Lin</name><name sortKey="Ping, Jia Fong" sort="Ping, Jia Fong" uniqKey="Ping J" first="Jia-Fong" last="Ping">Jia-Fong Ping</name><name sortKey="Tsai, Fuu Jen" sort="Tsai, Fuu Jen" uniqKey="Tsai F" first="Fuu-Jen" last="Tsai">Fuu-Jen Tsai</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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