Severe acute respiratory syndrome coronavirus nsp1 facilitates efficient propagation in cells through a specific translational shutoff of host mRNA.
Identifieur interne : 001326 ( PubMed/Corpus ); précédent : 001325; suivant : 001327Severe acute respiratory syndrome coronavirus nsp1 facilitates efficient propagation in cells through a specific translational shutoff of host mRNA.
Auteurs : Tomohisa Tanaka ; Wataru Kamitani ; Marta L. Dediego ; Luis Enjuanes ; Yoshiharu MatsuuraSource :
- Journal of virology [ 1098-5514 ] ; 2012.
English descriptors
- KwdEn :
- 5' Untranslated Regions, Cell Line, Gene Expression Regulation, Viral, HEK293 Cells, Humans, Inverted Repeat Sequences, Peptide Chain Elongation, Translational, RNA Replicase (genetics), RNA Replicase (metabolism), RNA, Messenger (genetics), RNA, Messenger (metabolism), RNA, Untranslated (metabolism), RNA, Viral (genetics), RNA, Viral (metabolism), Ribosome Subunits, Small, Eukaryotic (metabolism), SARS Virus (genetics), SARS Virus (metabolism), Severe Acute Respiratory Syndrome (genetics), Severe Acute Respiratory Syndrome (metabolism), Severe Acute Respiratory Syndrome (virology), Viral Nonstructural Proteins (genetics), Viral Nonstructural Proteins (metabolism), Virus Replication (genetics).
- MESH :
- chemical , genetics : RNA Replicase, RNA, Messenger, RNA, Viral, Viral Nonstructural Proteins.
- chemical , metabolism : RNA Replicase, RNA, Messenger, RNA, Untranslated, RNA, Viral, Viral Nonstructural Proteins.
- chemical : 5' Untranslated Regions.
- genetics : SARS Virus, Severe Acute Respiratory Syndrome, Virus Replication.
- metabolism : Ribosome Subunits, Small, Eukaryotic, SARS Virus, Severe Acute Respiratory Syndrome.
- virology : Severe Acute Respiratory Syndrome.
- Cell Line, Gene Expression Regulation, Viral, HEK293 Cells, Humans, Inverted Repeat Sequences, Peptide Chain Elongation, Translational.
Abstract
Severe acute respiratory syndrome (SARS) coronavirus (SCoV) is an enveloped virus containing a single-stranded, positive-sense RNA genome. Nine mRNAs carrying a set of common 5' and 3' untranslated regions (UTR) are synthesized from the incoming viral genomic RNA in cells infected with SCoV. A nonstructural SCoV nsp1 protein causes a severe translational shutoff by binding to the 40S ribosomal subunits. The nsp1-40S ribosome complex further induces an endonucleolytic cleavage near the 5'UTR of host mRNA. However, the mechanism by which SCoV viral proteins are efficiently produced in infected cells in which host protein synthesis is impaired by nsp1 is unknown. In this study, we investigated the role of the viral UTRs in evasion of the nsp1-mediated shutoff. Luciferase activities were significantly suppressed in cells expressing nsp1 together with the mRNA carrying a luciferase gene, while nsp1 failed to suppress luciferase activities of the mRNA flanked by the 5'UTR of SCoV. An RNA-protein binding assay and RNA decay assay revealed that nsp1 bound to stem-loop 1 (SL1) in the 5'UTR of SCoV RNA and that the specific interaction with nsp1 stabilized the mRNA carrying SL1. Furthermore, experiments using an SCoV replicon system showed that the specific interaction enhanced the SCoV replication. The specific interaction of nsp1 with SL1 is an important strategy to facilitate efficient viral gene expression in infected cells, in which nsp1 suppresses host gene expression. Our data indicate a novel mechanism of viral gene expression control by nsp1 and give new insight into understanding the pathogenesis of SARS.
DOI: 10.1128/JVI.01700-12
PubMed: 22855488
Links to Exploration step
pubmed:22855488Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Severe acute respiratory syndrome coronavirus nsp1 facilitates efficient propagation in cells through a specific translational shutoff of host mRNA.</title>
<author><name sortKey="Tanaka, Tomohisa" sort="Tanaka, Tomohisa" uniqKey="Tanaka T" first="Tomohisa" last="Tanaka">Tomohisa Tanaka</name>
<affiliation><nlm:affiliation>Global COE Program, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.</nlm:affiliation>
</affiliation>
</author>
<author><name sortKey="Kamitani, Wataru" sort="Kamitani, Wataru" uniqKey="Kamitani W" first="Wataru" last="Kamitani">Wataru Kamitani</name>
</author>
<author><name sortKey="Dediego, Marta L" sort="Dediego, Marta L" uniqKey="Dediego M" first="Marta L" last="Dediego">Marta L. Dediego</name>
</author>
<author><name sortKey="Enjuanes, Luis" sort="Enjuanes, Luis" uniqKey="Enjuanes L" first="Luis" last="Enjuanes">Luis Enjuanes</name>
</author>
<author><name sortKey="Matsuura, Yoshiharu" sort="Matsuura, Yoshiharu" uniqKey="Matsuura Y" first="Yoshiharu" last="Matsuura">Yoshiharu Matsuura</name>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">PubMed</idno>
<date when="2012">2012</date>
<idno type="RBID">pubmed:22855488</idno>
<idno type="pmid">22855488</idno>
<idno type="doi">10.1128/JVI.01700-12</idno>
<idno type="wicri:Area/PubMed/Corpus">001326</idno>
<idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001326</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en">Severe acute respiratory syndrome coronavirus nsp1 facilitates efficient propagation in cells through a specific translational shutoff of host mRNA.</title>
<author><name sortKey="Tanaka, Tomohisa" sort="Tanaka, Tomohisa" uniqKey="Tanaka T" first="Tomohisa" last="Tanaka">Tomohisa Tanaka</name>
<affiliation><nlm:affiliation>Global COE Program, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.</nlm:affiliation>
</affiliation>
</author>
<author><name sortKey="Kamitani, Wataru" sort="Kamitani, Wataru" uniqKey="Kamitani W" first="Wataru" last="Kamitani">Wataru Kamitani</name>
</author>
<author><name sortKey="Dediego, Marta L" sort="Dediego, Marta L" uniqKey="Dediego M" first="Marta L" last="Dediego">Marta L. Dediego</name>
</author>
<author><name sortKey="Enjuanes, Luis" sort="Enjuanes, Luis" uniqKey="Enjuanes L" first="Luis" last="Enjuanes">Luis Enjuanes</name>
</author>
<author><name sortKey="Matsuura, Yoshiharu" sort="Matsuura, Yoshiharu" uniqKey="Matsuura Y" first="Yoshiharu" last="Matsuura">Yoshiharu Matsuura</name>
</author>
</analytic>
<series><title level="j">Journal of virology</title>
<idno type="eISSN">1098-5514</idno>
<imprint><date when="2012" type="published">2012</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>5' Untranslated Regions</term>
<term>Cell Line</term>
<term>Gene Expression Regulation, Viral</term>
<term>HEK293 Cells</term>
<term>Humans</term>
<term>Inverted Repeat Sequences</term>
<term>Peptide Chain Elongation, Translational</term>
<term>RNA Replicase (genetics)</term>
<term>RNA Replicase (metabolism)</term>
<term>RNA, Messenger (genetics)</term>
<term>RNA, Messenger (metabolism)</term>
<term>RNA, Untranslated (metabolism)</term>
<term>RNA, Viral (genetics)</term>
<term>RNA, Viral (metabolism)</term>
<term>Ribosome Subunits, Small, Eukaryotic (metabolism)</term>
<term>SARS Virus (genetics)</term>
<term>SARS Virus (metabolism)</term>
<term>Severe Acute Respiratory Syndrome (genetics)</term>
<term>Severe Acute Respiratory Syndrome (metabolism)</term>
<term>Severe Acute Respiratory Syndrome (virology)</term>
<term>Viral Nonstructural Proteins (genetics)</term>
<term>Viral Nonstructural Proteins (metabolism)</term>
<term>Virus Replication (genetics)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>RNA Replicase</term>
<term>RNA, Messenger</term>
<term>RNA, Viral</term>
<term>Viral Nonstructural Proteins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>RNA Replicase</term>
<term>RNA, Messenger</term>
<term>RNA, Untranslated</term>
<term>RNA, Viral</term>
<term>Viral Nonstructural Proteins</term>
</keywords>
<keywords scheme="MESH" type="chemical" xml:lang="en"><term>5' Untranslated Regions</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>SARS Virus</term>
<term>Severe Acute Respiratory Syndrome</term>
<term>Virus Replication</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Ribosome Subunits, Small, Eukaryotic</term>
<term>SARS Virus</term>
<term>Severe Acute Respiratory Syndrome</term>
</keywords>
<keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Cell Line</term>
<term>Gene Expression Regulation, Viral</term>
<term>HEK293 Cells</term>
<term>Humans</term>
<term>Inverted Repeat Sequences</term>
<term>Peptide Chain Elongation, Translational</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Severe acute respiratory syndrome (SARS) coronavirus (SCoV) is an enveloped virus containing a single-stranded, positive-sense RNA genome. Nine mRNAs carrying a set of common 5' and 3' untranslated regions (UTR) are synthesized from the incoming viral genomic RNA in cells infected with SCoV. A nonstructural SCoV nsp1 protein causes a severe translational shutoff by binding to the 40S ribosomal subunits. The nsp1-40S ribosome complex further induces an endonucleolytic cleavage near the 5'UTR of host mRNA. However, the mechanism by which SCoV viral proteins are efficiently produced in infected cells in which host protein synthesis is impaired by nsp1 is unknown. In this study, we investigated the role of the viral UTRs in evasion of the nsp1-mediated shutoff. Luciferase activities were significantly suppressed in cells expressing nsp1 together with the mRNA carrying a luciferase gene, while nsp1 failed to suppress luciferase activities of the mRNA flanked by the 5'UTR of SCoV. An RNA-protein binding assay and RNA decay assay revealed that nsp1 bound to stem-loop 1 (SL1) in the 5'UTR of SCoV RNA and that the specific interaction with nsp1 stabilized the mRNA carrying SL1. Furthermore, experiments using an SCoV replicon system showed that the specific interaction enhanced the SCoV replication. The specific interaction of nsp1 with SL1 is an important strategy to facilitate efficient viral gene expression in infected cells, in which nsp1 suppresses host gene expression. Our data indicate a novel mechanism of viral gene expression control by nsp1 and give new insight into understanding the pathogenesis of SARS.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">22855488</PMID>
<DateCompleted><Year>2012</Year>
<Month>12</Month>
<Day>26</Day>
</DateCompleted>
<DateRevised><Year>2018</Year>
<Month>11</Month>
<Day>13</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1098-5514</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>86</Volume>
<Issue>20</Issue>
<PubDate><Year>2012</Year>
<Month>Oct</Month>
</PubDate>
</JournalIssue>
<Title>Journal of virology</Title>
<ISOAbbreviation>J. Virol.</ISOAbbreviation>
</Journal>
<ArticleTitle>Severe acute respiratory syndrome coronavirus nsp1 facilitates efficient propagation in cells through a specific translational shutoff of host mRNA.</ArticleTitle>
<Pagination><MedlinePgn>11128-37</MedlinePgn>
</Pagination>
<Abstract><AbstractText>Severe acute respiratory syndrome (SARS) coronavirus (SCoV) is an enveloped virus containing a single-stranded, positive-sense RNA genome. Nine mRNAs carrying a set of common 5' and 3' untranslated regions (UTR) are synthesized from the incoming viral genomic RNA in cells infected with SCoV. A nonstructural SCoV nsp1 protein causes a severe translational shutoff by binding to the 40S ribosomal subunits. The nsp1-40S ribosome complex further induces an endonucleolytic cleavage near the 5'UTR of host mRNA. However, the mechanism by which SCoV viral proteins are efficiently produced in infected cells in which host protein synthesis is impaired by nsp1 is unknown. In this study, we investigated the role of the viral UTRs in evasion of the nsp1-mediated shutoff. Luciferase activities were significantly suppressed in cells expressing nsp1 together with the mRNA carrying a luciferase gene, while nsp1 failed to suppress luciferase activities of the mRNA flanked by the 5'UTR of SCoV. An RNA-protein binding assay and RNA decay assay revealed that nsp1 bound to stem-loop 1 (SL1) in the 5'UTR of SCoV RNA and that the specific interaction with nsp1 stabilized the mRNA carrying SL1. Furthermore, experiments using an SCoV replicon system showed that the specific interaction enhanced the SCoV replication. The specific interaction of nsp1 with SL1 is an important strategy to facilitate efficient viral gene expression in infected cells, in which nsp1 suppresses host gene expression. Our data indicate a novel mechanism of viral gene expression control by nsp1 and give new insight into understanding the pathogenesis of SARS.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Tanaka</LastName>
<ForeName>Tomohisa</ForeName>
<Initials>T</Initials>
<AffiliationInfo><Affiliation>Global COE Program, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kamitani</LastName>
<ForeName>Wataru</ForeName>
<Initials>W</Initials>
</Author>
<Author ValidYN="Y"><LastName>DeDiego</LastName>
<ForeName>Marta L</ForeName>
<Initials>ML</Initials>
</Author>
<Author ValidYN="Y"><LastName>Enjuanes</LastName>
<ForeName>Luis</ForeName>
<Initials>L</Initials>
</Author>
<Author ValidYN="Y"><LastName>Matsuura</LastName>
<ForeName>Yoshiharu</ForeName>
<Initials>Y</Initials>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>P01 AI060699</GrantID>
<Acronym>AI</Acronym>
<Agency>NIAID NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>2P01AI060699-06A1</GrantID>
<Acronym>AI</Acronym>
<Agency>NIAID NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>W000306844</GrantID>
<Agency>PHS HHS</Agency>
<Country>United States</Country>
</Grant>
</GrantList>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2012</Year>
<Month>08</Month>
<Day>01</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>J Virol</MedlineTA>
<NlmUniqueID>0113724</NlmUniqueID>
<ISSNLinking>0022-538X</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D020121">5' Untranslated Regions</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D012333">RNA, Messenger</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D022661">RNA, Untranslated</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D012367">RNA, Viral</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D017361">Viral Nonstructural Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.7.48</RegistryNumber>
<NameOfSubstance UI="C521592">Nsp1 protein, SARS coronavirus</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.7.48</RegistryNumber>
<NameOfSubstance UI="D012324">RNA Replicase</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D020121" MajorTopicYN="N">5' Untranslated Regions</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015967" MajorTopicYN="N">Gene Expression Regulation, Viral</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D057809" MajorTopicYN="N">HEK293 Cells</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D055029" MajorTopicYN="N">Inverted Repeat Sequences</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D010441" MajorTopicYN="Y">Peptide Chain Elongation, Translational</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D012324" MajorTopicYN="N">RNA Replicase</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D012333" MajorTopicYN="N">RNA, Messenger</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D022661" MajorTopicYN="N">RNA, Untranslated</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D012367" MajorTopicYN="N">RNA, Viral</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D054682" MajorTopicYN="N">Ribosome Subunits, Small, Eukaryotic</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D045473" MajorTopicYN="N">SARS Virus</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D045169" MajorTopicYN="N">Severe Acute Respiratory Syndrome</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000821" MajorTopicYN="Y">virology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D017361" MajorTopicYN="N">Viral Nonstructural Proteins</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D014779" MajorTopicYN="N">Virus Replication</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
</MeshHeadingList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2012</Year>
<Month>8</Month>
<Day>3</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed"><Year>2012</Year>
<Month>8</Month>
<Day>3</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>2012</Year>
<Month>12</Month>
<Day>27</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="pubmed">22855488</ArticleId>
<ArticleId IdType="pii">JVI.01700-12</ArticleId>
<ArticleId IdType="doi">10.1128/JVI.01700-12</ArticleId>
<ArticleId IdType="pmc">PMC3457165</ArticleId>
</ArticleIdList>
<ReferenceList><Reference><Citation>Virology. 2001 Mar 15;281(2):272-80</Citation>
<ArticleIdList><ArticleId IdType="pubmed">11277699</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cell. 2000 Sep 29;103(1):29-40</Citation>
<ArticleIdList><ArticleId IdType="pubmed">11051545</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Trends Biochem Sci. 2003 Mar;28(3):130-6</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12633992</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>N Engl J Med. 2003 May 15;348(20):1995-2005</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12671061</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>N Engl J Med. 2003 May 15;348(20):1967-76</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12690091</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>N Engl J Med. 2003 May 15;348(20):1953-66</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12690092</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Virol. 2003 Jun;77(12):6720-30</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12767992</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Gen Virol. 2003 Sep;84(Pt 9):2305-15</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12917450</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Virol. 2004 Jan;78(2):980-94</Citation>
<ArticleIdList><ArticleId IdType="pubmed">14694129</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Virol. 2004 Sep;78(18):9977-86</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15331731</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>EMBO J. 1996 Dec 16;15(24):7147-55</Citation>
<ArticleIdList><ArticleId IdType="pubmed">9003790</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Proc Natl Acad Sci U S A. 1997 Sep 2;94(18):9544-9</Citation>
<ArticleIdList><ArticleId IdType="pubmed">9275159</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Virol. 2005 Nov;79(21):13399-411</Citation>
<ArticleIdList><ArticleId IdType="pubmed">16227261</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Virol. 2005 Dec;79(24):15189-98</Citation>
<ArticleIdList><ArticleId IdType="pubmed">16306590</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Virol. 2005 Dec;79(24):15199-208</Citation>
<ArticleIdList><ArticleId IdType="pubmed">16306591</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Virus Res. 2006 Jul;119(1):76-88</Citation>
<ArticleIdList><ArticleId IdType="pubmed">16303201</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Proc Natl Acad Sci U S A. 2006 Aug 22;103(34):12885-90</Citation>
<ArticleIdList><ArticleId IdType="pubmed">16912115</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Virol. 2006 Nov;80(21):10600-14</Citation>
<ArticleIdList><ArticleId IdType="pubmed">16920822</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Virol. 2006 Nov;80(21):10900-6</Citation>
<ArticleIdList><ArticleId IdType="pubmed">16928748</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Virol. 2007 Apr;81(7):3151-61</Citation>
<ArticleIdList><ArticleId IdType="pubmed">17202208</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Virol. 2007 Nov;81(21):11620-33</Citation>
<ArticleIdList><ArticleId IdType="pubmed">17715225</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Mol Biol. 2008 Mar 28;377(3):790-803</Citation>
<ArticleIdList><ArticleId IdType="pubmed">18289557</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Virol. 2008 May;82(9):4471-9</Citation>
<ArticleIdList><ArticleId IdType="pubmed">18305050</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cell Cycle. 2009 May 1;8(9):1332-7</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19342890</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Virol. 2009 May;83(10):5282-8</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19264783</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Virol. 2009 Jun;83(12):6087-97</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19357173</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nat Struct Mol Biol. 2009 Nov;16(11):1134-40</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19838190</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Virology. 2010 May 25;401(1):29-41</Citation>
<ArticleIdList><ArticleId IdType="pubmed">20202661</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>FEBS Lett. 2011 Apr 6;585(7):1049-53</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21382373</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>PLoS Pathog. 2011 May;7(5):e1002059</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21637813</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Virol. 2011 Jul;85(13):6381-9</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21507972</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>PLoS Pathog. 2011 Oct;7(10):e1002294</Citation>
<ArticleIdList><ArticleId IdType="pubmed">22022266</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>PLoS Pathog. 2011 Dec;7(12):e1002433</Citation>
<ArticleIdList><ArticleId IdType="pubmed">22174690</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nucleic Acids Res. 2012 Jun;40(11):5065-77</Citation>
<ArticleIdList><ArticleId IdType="pubmed">22362731</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Virol. 2005 Feb;79(4):2506-16</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15681451</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Virol. 2000 Jun;74(11):5053-65</Citation>
<ArticleIdList><ArticleId IdType="pubmed">10799579</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Virol. 2000 Aug;74(15):7064-71</Citation>
<ArticleIdList><ArticleId IdType="pubmed">10888646</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Virol. 2000 Sep;74(17):8127-34</Citation>
<ArticleIdList><ArticleId IdType="pubmed">10933723</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>EMBO J. 2000 Sep 1;19(17):4701-11</Citation>
<ArticleIdList><ArticleId IdType="pubmed">10970862</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Virology. 2002 Nov 10;303(1):58-68</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12482658</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
</PubmedData>
</pubmed>
</record>
Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Sante/explor/SrasV1/Data/PubMed/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 001326 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/PubMed/Corpus/biblio.hfd -nk 001326 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien |wiki= Sante |area= SrasV1 |flux= PubMed |étape= Corpus |type= RBID |clé= pubmed:22855488 |texte= Severe acute respiratory syndrome coronavirus nsp1 facilitates efficient propagation in cells through a specific translational shutoff of host mRNA. }}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Corpus/RBID.i -Sk "pubmed:22855488" \ | HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Corpus/biblio.hfd \ | NlmPubMed2Wicri -a SrasV1
![]() | This area was generated with Dilib version V0.6.33. | ![]() |