Nucleocapsid protein of SARS-CoV activates interleukin-6 expression through cellular transcription factor NF-kappaB.
Identifieur interne : 001E24 ( PubMed/Corpus ); précédent : 001E23; suivant : 001E25Nucleocapsid protein of SARS-CoV activates interleukin-6 expression through cellular transcription factor NF-kappaB.
Auteurs : Xue Zhang ; Kailang Wu ; Di Wang ; Xin Yue ; Degui Song ; Ying Zhu ; Jianguo WuSource :
- Virology [ 0042-6822 ] ; 2007.
English descriptors
- KwdEn :
- Artificial Gene Fusion, Cell Line, Cell Nucleus (chemistry), Cytoplasm (chemistry), Electrophoretic Mobility Shift Assay, Epithelial Cells (virology), Genes, Reporter, Humans, Immunoprecipitation, Interleukin-6 (genetics), Luciferases (analysis), Luciferases (genetics), Lung (immunology), Lung (virology), Mutation, NF-kappa B (metabolism), Nucleocapsid Proteins (immunology), Nucleocapsid Proteins (metabolism), Protein Binding, Protein Transport, SARS Virus (immunology), Sequence Deletion.
- MESH :
- chemical , analysis : Luciferases.
- chemical , genetics : Interleukin-6, Luciferases.
- chemistry : Cell Nucleus, Cytoplasm.
- immunology : Lung, Nucleocapsid Proteins, SARS Virus.
- chemical , metabolism : NF-kappa B, Nucleocapsid Proteins.
- virology : Epithelial Cells, Lung.
- Artificial Gene Fusion, Cell Line, Electrophoretic Mobility Shift Assay, Genes, Reporter, Humans, Immunoprecipitation, Mutation, Protein Binding, Protein Transport, Sequence Deletion.
Abstract
High levels of interleukin-6 (IL-6) in the acute stage associated with lung lesions were found in SARS patients. To evaluate the mechanisms behind this event, we investigated the roles of SARS-CoV proteins in the regulation of IL-6. Results showed that the viral nucleocapsid (N) protein activated IL-6 expression in a concentration-dependent manner. Promoter analyses suggested that NF-kappaB binding element was required for IL-6 expression regulated by N protein. Further studies demonstrated that N protein bound directly to NF-kappaB element on the promoter. We also showed that N protein activated IL-6 expression through NF-kappaB by facilitating the translocation of NF-kappaB from cytosol to nucleus. Mutational analyses revealed that two regions of N protein were essential for its function in the activation of IL-6. These results provided new insights into understanding the mechanism involved in the function of SARS-CoV N protein and pathogenesis of the virus.
DOI: 10.1016/j.virol.2007.04.009
PubMed: 17490702
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pubmed:17490702Le document en format XML
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uniqKey="Zhu Y" first="Ying" last="Zhu">Ying Zhu</name></author><author><name sortKey="Wu, Jianguo" sort="Wu, Jianguo" uniqKey="Wu J" first="Jianguo" last="Wu">Jianguo Wu</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2007">2007</date><idno type="RBID">pubmed:17490702</idno><idno type="pmid">17490702</idno><idno type="doi">10.1016/j.virol.2007.04.009</idno><idno type="wicri:Area/PubMed/Corpus">001E24</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001E24</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Nucleocapsid protein of SARS-CoV activates interleukin-6 expression through cellular transcription factor NF-kappaB.</title><author><name sortKey="Zhang, Xue" sort="Zhang, Xue" uniqKey="Zhang X" first="Xue" last="Zhang">Xue Zhang</name><affiliation><nlm:affiliation>State Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan 430072, PR China.</nlm:affiliation></affiliation></author><author><name sortKey="Wu, Kailang" sort="Wu, Kailang" uniqKey="Wu K" first="Kailang" last="Wu">Kailang Wu</name></author><author><name sortKey="Wang, Di" sort="Wang, Di" uniqKey="Wang D" first="Di" last="Wang">Di Wang</name></author><author><name sortKey="Yue, Xin" sort="Yue, Xin" uniqKey="Yue X" first="Xin" last="Yue">Xin Yue</name></author><author><name sortKey="Song, Degui" sort="Song, Degui" uniqKey="Song D" first="Degui" last="Song">Degui Song</name></author><author><name sortKey="Zhu, Ying" sort="Zhu, Ying" uniqKey="Zhu Y" first="Ying" last="Zhu">Ying Zhu</name></author><author><name sortKey="Wu, Jianguo" sort="Wu, Jianguo" uniqKey="Wu J" first="Jianguo" last="Wu">Jianguo Wu</name></author></analytic><series><title level="j">Virology</title><idno type="ISSN">0042-6822</idno><imprint><date when="2007" type="published">2007</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Artificial Gene Fusion</term><term>Cell Line</term><term>Cell Nucleus (chemistry)</term><term>Cytoplasm (chemistry)</term><term>Electrophoretic Mobility Shift Assay</term><term>Epithelial Cells (virology)</term><term>Genes, Reporter</term><term>Humans</term><term>Immunoprecipitation</term><term>Interleukin-6 (genetics)</term><term>Luciferases (analysis)</term><term>Luciferases (genetics)</term><term>Lung (immunology)</term><term>Lung (virology)</term><term>Mutation</term><term>NF-kappa B (metabolism)</term><term>Nucleocapsid Proteins (immunology)</term><term>Nucleocapsid Proteins (metabolism)</term><term>Protein Binding</term><term>Protein Transport</term><term>SARS Virus (immunology)</term><term>Sequence Deletion</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>Luciferases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Interleukin-6</term><term>Luciferases</term></keywords><keywords scheme="MESH" qualifier="chemistry" xml:lang="en"><term>Cell Nucleus</term><term>Cytoplasm</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Lung</term><term>Nucleocapsid Proteins</term><term>SARS Virus</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>NF-kappa B</term><term>Nucleocapsid Proteins</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Epithelial Cells</term><term>Lung</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Artificial Gene Fusion</term><term>Cell Line</term><term>Electrophoretic Mobility Shift Assay</term><term>Genes, Reporter</term><term>Humans</term><term>Immunoprecipitation</term><term>Mutation</term><term>Protein Binding</term><term>Protein Transport</term><term>Sequence Deletion</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">High levels of interleukin-6 (IL-6) in the acute stage associated with lung lesions were found in SARS patients. To evaluate the mechanisms behind this event, we investigated the roles of SARS-CoV proteins in the regulation of IL-6. Results showed that the viral nucleocapsid (N) protein activated IL-6 expression in a concentration-dependent manner. Promoter analyses suggested that NF-kappaB binding element was required for IL-6 expression regulated by N protein. Further studies demonstrated that N protein bound directly to NF-kappaB element on the promoter. We also showed that N protein activated IL-6 expression through NF-kappaB by facilitating the translocation of NF-kappaB from cytosol to nucleus. Mutational analyses revealed that two regions of N protein were essential for its function in the activation of IL-6. These results provided new insights into understanding the mechanism involved in the function of SARS-CoV N protein and pathogenesis of the virus.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">17490702</PMID><DateCompleted><Year>2007</Year><Month>09</Month><Day>27</Day></DateCompleted><DateRevised><Year>2020</Year><Month>04</Month><Day>07</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0042-6822</ISSN><JournalIssue CitedMedium="Print"><Volume>365</Volume><Issue>2</Issue><PubDate><Year>2007</Year><Month>Sep</Month><Day>01</Day></PubDate></JournalIssue><Title>Virology</Title><ISOAbbreviation>Virology</ISOAbbreviation></Journal><ArticleTitle>Nucleocapsid protein of SARS-CoV activates interleukin-6 expression through cellular transcription factor NF-kappaB.</ArticleTitle><Pagination><MedlinePgn>324-35</MedlinePgn></Pagination><Abstract><AbstractText>High levels of interleukin-6 (IL-6) in the acute stage associated with lung lesions were found in SARS patients. To evaluate the mechanisms behind this event, we investigated the roles of SARS-CoV proteins in the regulation of IL-6. Results showed that the viral nucleocapsid (N) protein activated IL-6 expression in a concentration-dependent manner. Promoter analyses suggested that NF-kappaB binding element was required for IL-6 expression regulated by N protein. Further studies demonstrated that N protein bound directly to NF-kappaB element on the promoter. We also showed that N protein activated IL-6 expression through NF-kappaB by facilitating the translocation of NF-kappaB from cytosol to nucleus. Mutational analyses revealed that two regions of N protein were essential for its function in the activation of IL-6. These results provided new insights into understanding the mechanism involved in the function of SARS-CoV N protein and pathogenesis of the virus.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Xue</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>State Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan 430072, PR China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wu</LastName><ForeName>Kailang</ForeName><Initials>K</Initials></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Di</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Yue</LastName><ForeName>Xin</ForeName><Initials>X</Initials></Author><Author ValidYN="Y"><LastName>Song</LastName><ForeName>Degui</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Zhu</LastName><ForeName>Ying</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Wu</LastName><ForeName>Jianguo</ForeName><Initials>J</Initials></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>2007</Year><Month>05</Month><Day>09</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Virology</MedlineTA><NlmUniqueID>0110674</NlmUniqueID><ISSNLinking>0042-6822</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015850">Interleukin-6</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016328">NF-kappa B</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D019590">Nucleocapsid 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