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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Severe acute respiratory syndrome coronavirus nsp1 protein suppresses host gene expression by promoting host mRNA degradation</title><author><name sortKey="Kamitani, Wataru" sort="Kamitani, Wataru" uniqKey="Kamitani W" first="Wataru" last="Kamitani">Wataru Kamitani</name><affiliation><nlm:aff id="aff1">*Departments of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555-1019; and</nlm:aff></affiliation></author><author><name sortKey="Narayanan, Krishna" sort="Narayanan, Krishna" uniqKey="Narayanan K" first="Krishna" last="Narayanan">Krishna Narayanan</name><affiliation><nlm:aff id="aff1">*Departments of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555-1019; and</nlm:aff></affiliation></author><author><name sortKey="Huang, Cheng" sort="Huang, Cheng" uniqKey="Huang C" first="Cheng" last="Huang">Cheng Huang</name><affiliation><nlm:aff id="aff1">*Departments of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555-1019; and</nlm:aff></affiliation></author><author><name sortKey="Lokugamage, Kumari" sort="Lokugamage, Kumari" uniqKey="Lokugamage K" first="Kumari" last="Lokugamage">Kumari Lokugamage</name><affiliation><nlm:aff id="aff1">*Departments of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555-1019; and</nlm:aff></affiliation></author><author><name sortKey="Ikegami, Tetsuro" sort="Ikegami, Tetsuro" uniqKey="Ikegami T" first="Tetsuro" last="Ikegami">Tetsuro Ikegami</name><affiliation><nlm:aff id="aff1">*Departments of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555-1019; and</nlm:aff></affiliation></author><author><name sortKey="Ito, Naoto" sort="Ito, Naoto" uniqKey="Ito N" first="Naoto" last="Ito">Naoto Ito</name><affiliation><nlm:aff id="aff1">*Departments of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555-1019; and</nlm:aff></affiliation><affiliation><nlm:aff id="aff2">Laboratory of Zoonotic Diseases, Division of Veterinary Medicine, Faculty of Applied Biological Science, Gifu University, 1-1 Yanagido, Gifu 501-1193, Japan</nlm:aff></affiliation></author><author><name sortKey="Kubo, Hideyuki" sort="Kubo, Hideyuki" uniqKey="Kubo H" first="Hideyuki" last="Kubo">Hideyuki Kubo</name><affiliation><nlm:aff id="aff1">*Departments of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555-1019; and</nlm:aff></affiliation></author><author><name sortKey="Makino, Shinji" sort="Makino, Shinji" uniqKey="Makino S" first="Shinji" last="Makino">Shinji Makino</name><affiliation><nlm:aff id="aff1">*Departments of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555-1019; and</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">16912115</idno><idno type="pmc">1568942</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1568942</idno><idno type="RBID">PMC:1568942</idno><idno type="doi">10.1073/pnas.0603144103</idno><date when="2006">2006</date><idno type="wicri:Area/Pmc/Corpus">000D22</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000D22</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Severe acute respiratory syndrome coronavirus nsp1 protein suppresses host gene expression by promoting host mRNA degradation</title><author><name sortKey="Kamitani, Wataru" sort="Kamitani, Wataru" uniqKey="Kamitani W" first="Wataru" last="Kamitani">Wataru Kamitani</name><affiliation><nlm:aff id="aff1">*Departments of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555-1019; and</nlm:aff></affiliation></author><author><name sortKey="Narayanan, Krishna" sort="Narayanan, Krishna" uniqKey="Narayanan K" first="Krishna" last="Narayanan">Krishna Narayanan</name><affiliation><nlm:aff id="aff1">*Departments of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555-1019; and</nlm:aff></affiliation></author><author><name sortKey="Huang, Cheng" sort="Huang, Cheng" uniqKey="Huang C" first="Cheng" last="Huang">Cheng Huang</name><affiliation><nlm:aff id="aff1">*Departments of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555-1019; and</nlm:aff></affiliation></author><author><name sortKey="Lokugamage, Kumari" sort="Lokugamage, Kumari" uniqKey="Lokugamage K" first="Kumari" last="Lokugamage">Kumari Lokugamage</name><affiliation><nlm:aff id="aff1">*Departments of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555-1019; and</nlm:aff></affiliation></author><author><name sortKey="Ikegami, Tetsuro" sort="Ikegami, Tetsuro" uniqKey="Ikegami T" first="Tetsuro" last="Ikegami">Tetsuro Ikegami</name><affiliation><nlm:aff id="aff1">*Departments of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555-1019; and</nlm:aff></affiliation></author><author><name sortKey="Ito, Naoto" sort="Ito, Naoto" uniqKey="Ito N" first="Naoto" last="Ito">Naoto Ito</name><affiliation><nlm:aff id="aff1">*Departments of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555-1019; and</nlm:aff></affiliation><affiliation><nlm:aff id="aff2">Laboratory of Zoonotic Diseases, Division of Veterinary Medicine, Faculty of Applied Biological Science, Gifu University, 1-1 Yanagido, Gifu 501-1193, Japan</nlm:aff></affiliation></author><author><name sortKey="Kubo, Hideyuki" sort="Kubo, Hideyuki" uniqKey="Kubo H" first="Hideyuki" last="Kubo">Hideyuki Kubo</name><affiliation><nlm:aff id="aff1">*Departments of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555-1019; and</nlm:aff></affiliation></author><author><name sortKey="Makino, Shinji" sort="Makino, Shinji" uniqKey="Makino S" first="Shinji" last="Makino">Shinji Makino</name><affiliation><nlm:aff id="aff1">*Departments of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555-1019; and</nlm:aff></affiliation></author></analytic><series><title level="j">Proceedings of the National Academy of Sciences of the United States of America</title><idno type="ISSN">0027-8424</idno><idno type="eISSN">1091-6490</idno><imprint><date when="2006">2006</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Severe acute respiratory syndrome (SARS) coronavirus (SCoV) causes a recently emerged human disease associated with pneumonia. The 5′ end two-thirds of the single-stranded positive-sense viral genomic RNA, gene 1, encodes 16 mature proteins. Expression of nsp1, the most N-terminal gene 1 protein, prevented Sendai virus-induced endogenous IFN-β mRNA accumulation without inhibiting dimerization of IFN regulatory factor 3, a protein that is essential for activation of the IFN-β promoter. Furthermore, nsp1 expression promoted degradation of expressed RNA transcripts and host endogenous mRNAs, leading to a strong host protein synthesis inhibition. SCoV replication also promoted degradation of expressed RNA transcripts and host mRNAs, suggesting that nsp1 exerted its mRNA destabilization function in infected cells. In contrast to nsp1-induced mRNA destablization, no degradation of the 28S and 18S rRNAs occurred in either nsp1-expressing cells or SCoV-infected cells. These data suggested that, in infected cells, nsp1 promotes host mRNA degradation and thereby suppresses host gene expression, including proteins involved in host innate immune functions. SCoV nsp1-mediated promotion of host mRNA degradation may play an important role in SCoV pathogenesis.</p></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Proc Natl Acad Sci U S A</journal-id><journal-id journal-id-type="publisher-id">PNAS</journal-id><journal-title>Proceedings of the National Academy of Sciences of the United States of America</journal-title><issn pub-type="ppub">0027-8424</issn><issn pub-type="epub">1091-6490</issn><publisher><publisher-name>National Academy of Sciences</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">16912115</article-id><article-id pub-id-type="pmc">1568942</article-id><article-id pub-id-type="publisher-id">3162</article-id><article-id pub-id-type="doi">10.1073/pnas.0603144103</article-id><article-categories><subj-group subj-group-type="heading"><subject>Biological Sciences</subject><subj-group><subject>Microbiology</subject></subj-group></subj-group></article-categories><title-group><article-title>Severe acute respiratory syndrome coronavirus nsp1 protein suppresses host gene expression by promoting host mRNA degradation</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Kamitani</surname><given-names>Wataru</given-names></name><xref rid="aff1" ref-type="aff">*</xref></contrib><contrib contrib-type="author"><name><surname>Narayanan</surname><given-names>Krishna</given-names></name><xref rid="aff1" ref-type="aff">*</xref></contrib><contrib contrib-type="author"><name><surname>Huang</surname><given-names>Cheng</given-names></name><xref rid="aff1" ref-type="aff">*</xref></contrib><contrib contrib-type="author"><name><surname>Lokugamage</surname><given-names>Kumari</given-names></name><xref rid="aff1" ref-type="aff">*</xref></contrib><contrib contrib-type="author"><name><surname>Ikegami</surname><given-names>Tetsuro</given-names></name><xref rid="aff1" ref-type="aff">*</xref></contrib><contrib contrib-type="author"><name><surname>Ito</surname><given-names>Naoto</given-names></name><xref rid="aff1" ref-type="aff">*</xref><xref rid="aff2" ref-type="aff"><sup>†</sup></xref></contrib><contrib contrib-type="author"><name><surname>Kubo</surname><given-names>Hideyuki</given-names></name><xref rid="aff1" ref-type="aff">*</xref></contrib><contrib contrib-type="author"><name><surname>Makino</surname><given-names>Shinji</given-names></name><xref rid="aff1" ref-type="aff">*</xref><xref ref-type="corresp" rid="cor1"><sup>‡</sup></xref></contrib><aff id="aff1">*Departments of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555-1019; and</aff><aff id="aff2"><sup>†</sup>Laboratory of Zoonotic Diseases, Division of Veterinary Medicine, Faculty of Applied Biological Science, Gifu University, 1-1 Yanagido, Gifu 501-1193, Japan</aff></contrib-group><author-notes><corresp id="cor1"><sup>‡</sup>To whom correspondence should be addressed. E-mail:
<email>shmakino@utmb.edu</email></corresp><fn fn-type="edited-by"><p>Edited by Peter Palese, Mount Sinai School of Medicine, New York, NY, and approved June 30, 2006</p></fn><fn fn-type="con"><p>Author contributions: W.K. and S.M. designed research; W.K., K.N., C.H., K.L., T.I., N.I., and H.K. performed research; C.H., K.L., T.I., and H.K. contributed new reagents/analytic tools; W.K. and S.M. analyzed data; and W.K. and S.M. wrote the paper.</p></fn><fn fn-type="conflict"><p>Conflict of interest statement: No conflicts declared.</p></fn></author-notes><pub-date pub-type="ppub"><day>22</day><month>8</month><year>2006</year></pub-date><pub-date pub-type="epub"><day>15</day><month>8</month><year>2006</year></pub-date><volume>103</volume><issue>34</issue><fpage>12885</fpage><lpage>12890</lpage><history><date date-type="received"><day>18</day><month>4</month><year>2006</year></date></history><copyright-statement>© 2006 by The National Academy of Sciences of the USA</copyright-statement><copyright-year>2006</copyright-year><abstract><p>Severe acute respiratory syndrome (SARS) coronavirus (SCoV) causes a recently emerged human disease associated with pneumonia. The 5′ end two-thirds of the single-stranded positive-sense viral genomic RNA, gene 1, encodes 16 mature proteins. Expression of nsp1, the most N-terminal gene 1 protein, prevented Sendai virus-induced endogenous IFN-β mRNA accumulation without inhibiting dimerization of IFN regulatory factor 3, a protein that is essential for activation of the IFN-β promoter. Furthermore, nsp1 expression promoted degradation of expressed RNA transcripts and host endogenous mRNAs, leading to a strong host protein synthesis inhibition. SCoV replication also promoted degradation of expressed RNA transcripts and host mRNAs, suggesting that nsp1 exerted its mRNA destabilization function in infected cells. In contrast to nsp1-induced mRNA destablization, no degradation of the 28S and 18S rRNAs occurred in either nsp1-expressing cells or SCoV-infected cells. These data suggested that, in infected cells, nsp1 promotes host mRNA degradation and thereby suppresses host gene expression, including proteins involved in host innate immune functions. SCoV nsp1-mediated promotion of host mRNA degradation may play an important role in SCoV pathogenesis.</p></abstract><kwd-group><kwd>virus virulence</kwd><kwd>SARS</kwd><kwd>mRNA stability</kwd><kwd>translation inhibition</kwd><kwd>innate immunity</kwd></kwd-group><custom-meta-wrap><custom-meta><meta-name>PDF</meta-name><meta-value><uri xlink:type="simple" xlink:href="zpq03406012885.pdf"></uri></meta-value></custom-meta></custom-meta-wrap></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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