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 : 001558 ( PubMed/Corpus ); précédent : 001557; suivant : 001559Severe 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 ; Chien-Chen Lai ; Jia-Fong Ping ; Fuu-Jen Tsai ; Lei Wan ; Ying-Ju Lin ; Szu-Hao Kung ; Cheng-Wen LinSource :
- The Journal of general virology [ 1465-2099 ] ; 2011.
English descriptors
- KwdEn :
- Cell Line, Cysteine Endopeptidases (metabolism), Down-Regulation, Humans, Interferon-alpha (antagonists & inhibitors), Interferon-alpha (immunology), Mitogen-Activated Protein Kinase 3 (antagonists & inhibitors), Monocytes (virology), Proteome (analysis), SARS Virus (immunology), SARS Virus (pathogenicity), Signal Transduction, Viral Proteins (metabolism).
- MESH :
- chemical , analysis : Proteome.
- chemical , antagonists & inhibitors : Interferon-alpha, Mitogen-Activated Protein Kinase 3.
- chemical , immunology : Interferon-alpha.
- chemical , metabolism : Cysteine Endopeptidases, Viral Proteins.
- immunology : SARS Virus.
- pathogenicity : SARS Virus.
- virology : Monocytes.
- Cell Line, Down-Regulation, Humans, Signal Transduction.
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.
DOI: 10.1099/vir.0.028936-0
PubMed: 21270289
Links to Exploration step
pubmed:21270289Le document en format XML
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Ping</name><affiliation><nlm:affiliation>Department of Medical Laboratory Science and Biotechnology, China Medical University, Taichung, Taiwan, ROC.</nlm:affiliation></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><nlm:affiliation>Department of Medical Genetics and Medical Research, China Medical University Hospital, Taichung, Taiwan, ROC.</nlm:affiliation></affiliation></author><author><name sortKey="Wan, Lei" sort="Wan, Lei" uniqKey="Wan L" first="Lei" last="Wan">Lei Wan</name><affiliation><nlm:affiliation>Department of Medical Genetics and Medical Research, China Medical University Hospital, Taichung, Taiwan, ROC.</nlm:affiliation></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><nlm:affiliation>Department of Medical Genetics and Medical Research, China Medical University Hospital, Taichung, Taiwan, ROC.</nlm:affiliation></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><nlm:affiliation>Department of Biotechnology and Laboratory Science in Medicine, National Yang Ming University, Taipei, Taiwan, ROC.</nlm:affiliation></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><nlm:affiliation>Department of Biotechnology, Asia University, Wufeng, Taichung, Taiwan, ROC.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2011">2011</date><idno type="RBID">pubmed:21270289</idno><idno type="pmid">21270289</idno><idno type="doi">10.1099/vir.0.028936-0</idno><idno type="wicri:Area/PubMed/Corpus">001558</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001558</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">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><nlm:affiliation>Institute of Molecular Biology, National Chung Hsing University, Taichung, Taiwan, ROC.</nlm:affiliation></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><nlm:affiliation>Department of Medical Genetics and Medical Research, China Medical University Hospital, Taichung, Taiwan, ROC.</nlm:affiliation></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><nlm:affiliation>Department of Medical Laboratory Science and Biotechnology, China Medical University, Taichung, Taiwan, ROC.</nlm:affiliation></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><nlm:affiliation>Department of Medical Genetics and Medical Research, China Medical University Hospital, Taichung, Taiwan, ROC.</nlm:affiliation></affiliation></author><author><name sortKey="Wan, Lei" sort="Wan, Lei" uniqKey="Wan L" first="Lei" last="Wan">Lei Wan</name><affiliation><nlm:affiliation>Department of Medical Genetics and Medical Research, China Medical University Hospital, Taichung, Taiwan, ROC.</nlm:affiliation></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><nlm:affiliation>Department of Medical Genetics and Medical Research, China Medical University Hospital, Taichung, Taiwan, ROC.</nlm:affiliation></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><nlm:affiliation>Department of Biotechnology and Laboratory Science in Medicine, National Yang Ming University, Taipei, Taiwan, ROC.</nlm:affiliation></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><nlm:affiliation>Department of Biotechnology, Asia University, Wufeng, Taichung, Taiwan, ROC.</nlm:affiliation></affiliation></author></analytic><series><title level="j">The Journal of general virology</title><idno type="eISSN">1465-2099</idno><imprint><date when="2011" type="published">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Cell Line</term><term>Cysteine Endopeptidases (metabolism)</term><term>Down-Regulation</term><term>Humans</term><term>Interferon-alpha (antagonists & inhibitors)</term><term>Interferon-alpha (immunology)</term><term>Mitogen-Activated Protein Kinase 3 (antagonists & inhibitors)</term><term>Monocytes (virology)</term><term>Proteome (analysis)</term><term>SARS Virus (immunology)</term><term>SARS Virus (pathogenicity)</term><term>Signal Transduction</term><term>Viral Proteins (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>Proteome</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Interferon-alpha</term><term>Mitogen-Activated Protein Kinase 3</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Interferon-alpha</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cysteine Endopeptidases</term><term>Viral Proteins</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Monocytes</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Line</term><term>Down-Regulation</term><term>Humans</term><term>Signal Transduction</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><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">21270289</PMID><DateCompleted><Year>2011</Year><Month>06</Month><Day>14</Day></DateCompleted><DateRevised><Year>2020</Year><Month>03</Month><Day>25</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1465-2099</ISSN><JournalIssue CitedMedium="Internet"><Volume>92</Volume><Issue>Pt 5</Issue><PubDate><Year>2011</Year><Month>May</Month></PubDate></JournalIssue><Title>The Journal of general virology</Title><ISOAbbreviation>J. Gen. Virol.</ISOAbbreviation></Journal><ArticleTitle>Severe acute respiratory syndrome coronavirus papain-like protease suppressed alpha interferon-induced responses through downregulation of extracellular signal-regulated kinase 1-mediated signalling pathways.</ArticleTitle><Pagination><MedlinePgn>1127-1140</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1099/vir.0.028936-0</ELocationID><Abstract><AbstractText>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.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Shih-Wein</ForeName><Initials>SW</Initials><AffiliationInfo><Affiliation>Institute of Molecular Biology, National Chung Hsing University, Taichung, Taiwan, ROC.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Medical Laboratory Science and Biotechnology, China Medical University, Taichung, Taiwan, ROC.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lai</LastName><ForeName>Chien-Chen</ForeName><Initials>CC</Initials><AffiliationInfo><Affiliation>Department of Medical Genetics and Medical Research, China Medical University Hospital, Taichung, Taiwan, ROC.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Institute of Molecular Biology, National Chung Hsing University, Taichung, Taiwan, ROC.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ping</LastName><ForeName>Jia-Fong</ForeName><Initials>JF</Initials><AffiliationInfo><Affiliation>Department of Medical Laboratory Science and Biotechnology, China Medical University, Taichung, Taiwan, ROC.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tsai</LastName><ForeName>Fuu-Jen</ForeName><Initials>FJ</Initials><AffiliationInfo><Affiliation>Department of Medical Genetics and Medical Research, China Medical University Hospital, Taichung, Taiwan, ROC.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wan</LastName><ForeName>Lei</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Medical Genetics and Medical Research, China Medical University Hospital, Taichung, Taiwan, ROC.</Affiliation></AffiliationInfo></Author><Author 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ROC.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Medical Laboratory Science and Biotechnology, China Medical University, Taichung, Taiwan, ROC.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2011</Year><Month>01</Month><Day>26</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>J Gen Virol</MedlineTA><NlmUniqueID>0077340</NlmUniqueID><ISSNLinking>0022-1317</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016898">Interferon-alpha</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance 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MajorTopicYN="Y">Down-Regulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016898" MajorTopicYN="N">Interferon-alpha</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="Y">antagonists & inhibitors</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D048052" MajorTopicYN="N">Mitogen-Activated Protein Kinase 3</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="Y">antagonists & inhibitors</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009000" MajorTopicYN="N">Monocytes</DescriptorName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020543" MajorTopicYN="N">Proteome</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D045473" MajorTopicYN="N">SARS Virus</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000472" MajorTopicYN="N">pathogenicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="Y">Signal Transduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014764" MajorTopicYN="N">Viral Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2011</Year><Month>1</Month><Day>29</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2011</Year><Month>1</Month><Day>29</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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