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 : 002284 ( Ncbi/Checkpoint ); précédent : 002283; suivant : 002285Severe 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 [République populaire de Chine] ; Chien-Chen Lai [République populaire de Chine] ; Jia-Fong Ping [République populaire de Chine] ; Fuu-Jen Tsai [République populaire de Chine] ; Lei Wan [République populaire de Chine] ; Ying-Ju Lin [République populaire de Chine] ; Szu-Hao Kung [République populaire de Chine] ; Cheng-Wen Lin [République populaire de Chine]Source :
- The Journal of general virology [ 1465-2099 ] ; 2011.
Descripteurs français
- KwdFr :
- Cysteine endopeptidases (métabolisme), Humains, Interféron alpha (antagonistes et inhibiteurs), Interféron alpha (immunologie), Lignée cellulaire, Mitogen-Activated Protein Kinase 3 (antagonistes et inhibiteurs), Monocytes (virologie), Protéines virales (métabolisme), Protéome (analyse), Régulation négative, Transduction du signal, Virus du SRAS (immunologie), Virus du SRAS (pathogénicité).
- MESH :
- analyse : Protéome.
- antagonistes et inhibiteurs : Interféron alpha, Mitogen-Activated Protein Kinase 3.
- immunologie : Interféron alpha, Virus du SRAS.
- métabolisme : Cysteine endopeptidases, Protéines virales.
- pathogénicité : Virus du SRAS.
- virologie : Monocytes.
- Humains, Lignée cellulaire, Régulation négative, Transduction du signal.
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
Affiliations:
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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"><nlm:affiliation>Institute of Molecular Biology, National Chung Hsing University, Taichung, Taiwan, ROC.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Institute of Molecular Biology, National Chung Hsing University, Taichung, Taiwan</wicri:regionArea><wicri:noRegion>Taiwan</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"><nlm:affiliation>Department of Medical Genetics and Medical Research, China Medical University Hospital, Taichung, Taiwan, ROC.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Medical Genetics and Medical Research, China Medical University Hospital, Taichung, Taiwan</wicri:regionArea><wicri:noRegion>Taiwan</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"><nlm:affiliation>Department of Medical Laboratory Science and Biotechnology, China Medical University, Taichung, Taiwan, ROC.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Medical Laboratory Science and Biotechnology, China Medical University, Taichung, Taiwan</wicri:regionArea><wicri:noRegion>Taiwan</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"><nlm:affiliation>Department of Medical Genetics and Medical Research, China Medical University Hospital, Taichung, 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Lin</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medical Genetics and Medical Research, China Medical University Hospital, Taichung, Taiwan, ROC.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Medical Genetics and Medical Research, China Medical University Hospital, Taichung, Taiwan</wicri:regionArea><wicri:noRegion>Taiwan</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"><nlm:affiliation>Department of Biotechnology and Laboratory Science in Medicine, National Yang Ming University, Taipei, Taiwan, ROC.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Biotechnology and Laboratory Science in Medicine, National Yang Ming University, Taipei, Taiwan</wicri:regionArea><wicri:noRegion>Taiwan</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"><nlm:affiliation>Department of Biotechnology, Asia University, Wufeng, Taichung, Taiwan, ROC.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Biotechnology, Asia University, Wufeng, Taichung, Taiwan</wicri:regionArea><wicri:noRegion>Taiwan</wicri:noRegion></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="KwdFr" xml:lang="fr"><term>Cysteine endopeptidases (métabolisme)</term><term>Humains</term><term>Interféron alpha (antagonistes et inhibiteurs)</term><term>Interféron alpha (immunologie)</term><term>Lignée cellulaire</term><term>Mitogen-Activated Protein Kinase 3 (antagonistes et inhibiteurs)</term><term>Monocytes (virologie)</term><term>Protéines virales (métabolisme)</term><term>Protéome (analyse)</term><term>Régulation négative</term><term>Transduction du signal</term><term>Virus du SRAS (immunologie)</term><term>Virus du SRAS (pathogénicité)</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="analyse" xml:lang="fr"><term>Protéome</term></keywords><keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Interféron alpha</term><term>Mitogen-Activated Protein Kinase 3</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Interféron alpha</term><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cysteine endopeptidases</term><term>Protéines virales</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Monocytes</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><keywords scheme="MESH" xml:lang="fr"><term>Humains</term><term>Lignée cellulaire</term><term>Régulation négative</term><term>Transduction du signal</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>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><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="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><name sortKey="Wan, Lei" sort="Wan, Lei" uniqKey="Wan L" first="Lei" last="Wan">Lei Wan</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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