SARS-coronavirus open reading frame-9b suppresses innate immunity by targeting mitochondria and the MAVS/TRAF3/TRAF6 signalosome.
Identifieur interne : 000F44 ( PubMed/Curation ); précédent : 000F43; suivant : 000F45SARS-coronavirus open reading frame-9b suppresses innate immunity by targeting mitochondria and the MAVS/TRAF3/TRAF6 signalosome.
Auteurs : Chong-Shan Shi [États-Unis] ; Hai-Yan Qi [États-Unis] ; Cedric Boularan [États-Unis] ; Ning-Na Huang [États-Unis] ; Mones Abu-Asab [États-Unis] ; James H. Shelhamer [États-Unis] ; John H. Kehrl [États-Unis]Source :
- Journal of immunology (Baltimore, Md. : 1950) [ 1550-6606 ] ; 2014.
Descripteurs français
- KwdFr :
- Autophagie (génétique), Cadres ouverts de lecture (génétique), Cadres ouverts de lecture (immunologie), Cellules HEK293, Facteur-3 associé aux récepteurs de TNF (métabolisme), Facteur-6 associé aux récepteurs de TNF (métabolisme), Humains, Immunité innée (génétique), Interférence par ARN, Lignée cellulaire, Mitochondries (génétique), Mitochondries (immunologie), Mitochondries (virologie), Petit ARN interférent, Protéine-5 associée à l'autophagie, Protéines adaptatrices de la transduction du signal (métabolisme), Protéines associées aux microtubules (biosynthèse), Protéines associées aux microtubules (génétique), Protéines associées aux microtubules (métabolisme), Protéines de liaison à l'ARN (biosynthèse), Protéines de liaison à l'ARN (génétique), Protéines de répression (biosynthèse), Protéines de répression (génétique), Protéines mitochondriales (génétique), Protéines mitochondriales (métabolisme), Protéines virales (génétique), Protéines virales (immunologie), Protéines à fluorescence verte, Syndrome respiratoire aigu sévère (immunologie), Syndrome respiratoire aigu sévère (virologie), Ubiquitin-protein ligases (biosynthèse), Ubiquitin-protein ligases (génétique), Ubiquitinylation, Virus du SRAS (génétique), Virus du SRAS (immunologie), dGTPases (génétique), dGTPases (métabolisme), Échappement immunitaire.
- MESH :
- biosynthèse : Protéines associées aux microtubules, Protéines de liaison à l'ARN, Protéines de répression, Ubiquitin-protein ligases.
- génétique : Autophagie, Cadres ouverts de lecture, Immunité innée, Mitochondries, Protéines associées aux microtubules, Protéines de liaison à l'ARN, Protéines de répression, Protéines mitochondriales, Protéines virales, Ubiquitin-protein ligases, Virus du SRAS, dGTPases.
- immunologie : Cadres ouverts de lecture, Mitochondries, Protéines virales, Syndrome respiratoire aigu sévère, Virus du SRAS.
- métabolisme : Facteur-3 associé aux récepteurs de TNF, Facteur-6 associé aux récepteurs de TNF, Protéines adaptatrices de la transduction du signal, Protéines associées aux microtubules, Protéines mitochondriales, dGTPases.
- virologie : Mitochondries, Syndrome respiratoire aigu sévère.
- Cellules HEK293, Humains, Interférence par ARN, Lignée cellulaire, Petit ARN interférent, Protéine-5 associée à l'autophagie, Protéines à fluorescence verte, Ubiquitinylation, Échappement immunitaire.
English descriptors
- KwdEn :
- Adaptor Proteins, Signal Transducing (metabolism), Autophagy (genetics), Autophagy-Related Protein 5, Cell Line, GTP Phosphohydrolases (genetics), GTP Phosphohydrolases (metabolism), Green Fluorescent Proteins, HEK293 Cells, Humans, Immune Evasion, Immunity, Innate (genetics), Microtubule-Associated Proteins (biosynthesis), Microtubule-Associated Proteins (genetics), Microtubule-Associated Proteins (metabolism), Mitochondria (genetics), Mitochondria (immunology), Mitochondria (virology), Mitochondrial Proteins (genetics), Mitochondrial Proteins (metabolism), Open Reading Frames (genetics), Open Reading Frames (immunology), RNA Interference, RNA, Small Interfering, RNA-Binding Proteins (biosynthesis), RNA-Binding Proteins (genetics), Repressor Proteins (biosynthesis), Repressor Proteins (genetics), SARS Virus (genetics), SARS Virus (immunology), Severe Acute Respiratory Syndrome (immunology), Severe Acute Respiratory Syndrome (virology), TNF Receptor-Associated Factor 3 (metabolism), TNF Receptor-Associated Factor 6 (metabolism), Ubiquitin-Protein Ligases (biosynthesis), Ubiquitin-Protein Ligases (genetics), Ubiquitination, Viral Proteins (genetics), Viral Proteins (immunology).
- MESH :
- chemical , biosynthesis : Microtubule-Associated Proteins, RNA-Binding Proteins, Repressor Proteins, Ubiquitin-Protein Ligases.
- chemical , genetics : GTP Phosphohydrolases, Microtubule-Associated Proteins, Mitochondrial Proteins, RNA-Binding Proteins, Repressor Proteins, Ubiquitin-Protein Ligases, Viral Proteins.
- chemical , immunology : Viral Proteins.
- chemical , metabolism : Adaptor Proteins, Signal Transducing, GTP Phosphohydrolases, Microtubule-Associated Proteins, Mitochondrial Proteins, TNF Receptor-Associated Factor 3, TNF Receptor-Associated Factor 6.
- genetics : Autophagy, Immunity, Innate, Mitochondria, Open Reading Frames, SARS Virus.
- immunology : Mitochondria, Open Reading Frames, SARS Virus, Severe Acute Respiratory Syndrome.
- virology : Mitochondria, Severe Acute Respiratory Syndrome.
- chemical : Autophagy-Related Protein 5, Cell Line, Green Fluorescent Proteins, HEK293 Cells, Humans, Immune Evasion, RNA Interference, RNA, Small Interfering, Ubiquitination.
Abstract
Coronaviruses (CoV) have recently emerged as potentially serious pathogens that can cause significant human morbidity and death. The severe acute respiratory syndrome (SARS)-CoV was identified as the etiologic agent of the 2002-2003 international SARS outbreak. Yet, how SARS evades innate immune responses to cause human disease remains poorly understood. In this study, we show that a protein encoded by SARS-CoV designated as open reading frame-9b (ORF-9b) localizes to mitochondria and causes mitochondrial elongation by triggering ubiquitination and proteasomal degradation of dynamin-like protein 1, a host protein involved in mitochondrial fission. Also, acting on mitochondria, ORF-9b targets the mitochondrial-associated adaptor molecule MAVS signalosome by usurping PCBP2 and the HECT domain E3 ligase AIP4 to trigger the degradation of MAVS, TRAF3, and TRAF 6. This severely limits host cell IFN responses. Reducing either PCBP2 or AIP4 expression substantially reversed the ORF-9b-mediated reduction of MAVS and the suppression of antiviral transcriptional responses. Finally, transient ORF-9b expression led to a strong induction of autophagy in cells. The induction of autophagy depended upon ATG5, a critical autophagy regulator, but the inhibition of MAVS signaling did not. These results indicate that SARS-CoV ORF-9b manipulates host cell mitochondria and mitochondrial function to help evade host innate immunity. This study has uncovered an important clue to the pathogenesis of SARS-CoV infection and illustrates the havoc that a small ORF can cause in cells.
DOI: 10.4049/jimmunol.1303196
PubMed: 25135833
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pubmed:25135833Le document en format XML
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<term>Autophagy (genetics)</term>
<term>Autophagy-Related Protein 5</term>
<term>Cell Line</term>
<term>GTP Phosphohydrolases (genetics)</term>
<term>GTP Phosphohydrolases (metabolism)</term>
<term>Green Fluorescent Proteins</term>
<term>HEK293 Cells</term>
<term>Humans</term>
<term>Immune Evasion</term>
<term>Immunity, Innate (genetics)</term>
<term>Microtubule-Associated Proteins (biosynthesis)</term>
<term>Microtubule-Associated Proteins (genetics)</term>
<term>Microtubule-Associated Proteins (metabolism)</term>
<term>Mitochondria (genetics)</term>
<term>Mitochondria (immunology)</term>
<term>Mitochondria (virology)</term>
<term>Mitochondrial Proteins (genetics)</term>
<term>Mitochondrial Proteins (metabolism)</term>
<term>Open Reading Frames (genetics)</term>
<term>Open Reading Frames (immunology)</term>
<term>RNA Interference</term>
<term>RNA, Small Interfering</term>
<term>RNA-Binding Proteins (biosynthesis)</term>
<term>RNA-Binding Proteins (genetics)</term>
<term>Repressor Proteins (biosynthesis)</term>
<term>Repressor Proteins (genetics)</term>
<term>SARS Virus (genetics)</term>
<term>SARS Virus (immunology)</term>
<term>Severe Acute Respiratory Syndrome (immunology)</term>
<term>Severe Acute Respiratory Syndrome (virology)</term>
<term>TNF Receptor-Associated Factor 3 (metabolism)</term>
<term>TNF Receptor-Associated Factor 6 (metabolism)</term>
<term>Ubiquitin-Protein Ligases (biosynthesis)</term>
<term>Ubiquitin-Protein Ligases (genetics)</term>
<term>Ubiquitination</term>
<term>Viral Proteins (genetics)</term>
<term>Viral Proteins (immunology)</term>
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<term>Cadres ouverts de lecture (génétique)</term>
<term>Cadres ouverts de lecture (immunologie)</term>
<term>Cellules HEK293</term>
<term>Facteur-3 associé aux récepteurs de TNF (métabolisme)</term>
<term>Facteur-6 associé aux récepteurs de TNF (métabolisme)</term>
<term>Humains</term>
<term>Immunité innée (génétique)</term>
<term>Interférence par ARN</term>
<term>Lignée cellulaire</term>
<term>Mitochondries (génétique)</term>
<term>Mitochondries (immunologie)</term>
<term>Mitochondries (virologie)</term>
<term>Petit ARN interférent</term>
<term>Protéine-5 associée à l'autophagie</term>
<term>Protéines adaptatrices de la transduction du signal (métabolisme)</term>
<term>Protéines associées aux microtubules (biosynthèse)</term>
<term>Protéines associées aux microtubules (génétique)</term>
<term>Protéines associées aux microtubules (métabolisme)</term>
<term>Protéines de liaison à l'ARN (biosynthèse)</term>
<term>Protéines de liaison à l'ARN (génétique)</term>
<term>Protéines de répression (biosynthèse)</term>
<term>Protéines de répression (génétique)</term>
<term>Protéines mitochondriales (génétique)</term>
<term>Protéines mitochondriales (métabolisme)</term>
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<term>Protéines virales (immunologie)</term>
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<term>Syndrome respiratoire aigu sévère (virologie)</term>
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<term>Ubiquitin-protein ligases (génétique)</term>
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<term>Virus du SRAS (génétique)</term>
<term>Virus du SRAS (immunologie)</term>
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<term>Repressor Proteins</term>
<term>Ubiquitin-Protein Ligases</term>
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<term>Microtubule-Associated Proteins</term>
<term>Mitochondrial Proteins</term>
<term>RNA-Binding Proteins</term>
<term>Repressor Proteins</term>
<term>Ubiquitin-Protein Ligases</term>
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<term>Microtubule-Associated Proteins</term>
<term>Mitochondrial Proteins</term>
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<term>TNF Receptor-Associated Factor 6</term>
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<term>Protéines de liaison à l'ARN</term>
<term>Protéines de répression</term>
<term>Ubiquitin-protein ligases</term>
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<term>Immunity, Innate</term>
<term>Mitochondria</term>
<term>Open Reading Frames</term>
<term>SARS Virus</term>
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<term>Cadres ouverts de lecture</term>
<term>Immunité innée</term>
<term>Mitochondries</term>
<term>Protéines associées aux microtubules</term>
<term>Protéines de liaison à l'ARN</term>
<term>Protéines de répression</term>
<term>Protéines mitochondriales</term>
<term>Protéines virales</term>
<term>Ubiquitin-protein ligases</term>
<term>Virus du SRAS</term>
<term>dGTPases</term>
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<term>Mitochondries</term>
<term>Protéines virales</term>
<term>Syndrome respiratoire aigu sévère</term>
<term>Virus du SRAS</term>
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<term>Open Reading Frames</term>
<term>SARS Virus</term>
<term>Severe Acute Respiratory Syndrome</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Facteur-3 associé aux récepteurs de TNF</term>
<term>Facteur-6 associé aux récepteurs de TNF</term>
<term>Protéines adaptatrices de la transduction du signal</term>
<term>Protéines associées aux microtubules</term>
<term>Protéines mitochondriales</term>
<term>dGTPases</term>
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<keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Mitochondries</term>
<term>Syndrome respiratoire aigu sévère</term>
</keywords>
<keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Mitochondria</term>
<term>Severe Acute Respiratory Syndrome</term>
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<keywords scheme="MESH" type="chemical" xml:lang="en"><term>Autophagy-Related Protein 5</term>
<term>Cell Line</term>
<term>Green Fluorescent Proteins</term>
<term>HEK293 Cells</term>
<term>Humans</term>
<term>Immune Evasion</term>
<term>RNA Interference</term>
<term>RNA, Small Interfering</term>
<term>Ubiquitination</term>
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<term>Humains</term>
<term>Interférence par ARN</term>
<term>Lignée cellulaire</term>
<term>Petit ARN interférent</term>
<term>Protéine-5 associée à l'autophagie</term>
<term>Protéines à fluorescence verte</term>
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<front><div type="abstract" xml:lang="en">Coronaviruses (CoV) have recently emerged as potentially serious pathogens that can cause significant human morbidity and death. The severe acute respiratory syndrome (SARS)-CoV was identified as the etiologic agent of the 2002-2003 international SARS outbreak. Yet, how SARS evades innate immune responses to cause human disease remains poorly understood. In this study, we show that a protein encoded by SARS-CoV designated as open reading frame-9b (ORF-9b) localizes to mitochondria and causes mitochondrial elongation by triggering ubiquitination and proteasomal degradation of dynamin-like protein 1, a host protein involved in mitochondrial fission. Also, acting on mitochondria, ORF-9b targets the mitochondrial-associated adaptor molecule MAVS signalosome by usurping PCBP2 and the HECT domain E3 ligase AIP4 to trigger the degradation of MAVS, TRAF3, and TRAF 6. This severely limits host cell IFN responses. Reducing either PCBP2 or AIP4 expression substantially reversed the ORF-9b-mediated reduction of MAVS and the suppression of antiviral transcriptional responses. Finally, transient ORF-9b expression led to a strong induction of autophagy in cells. The induction of autophagy depended upon ATG5, a critical autophagy regulator, but the inhibition of MAVS signaling did not. These results indicate that SARS-CoV ORF-9b manipulates host cell mitochondria and mitochondrial function to help evade host innate immunity. This study has uncovered an important clue to the pathogenesis of SARS-CoV infection and illustrates the havoc that a small ORF can cause in cells. </div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25135833</PMID>
<DateCompleted><Year>2014</Year>
<Month>11</Month>
<Day>25</Day>
</DateCompleted>
<DateRevised><Year>2019</Year>
<Month>10</Month>
<Day>08</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1550-6606</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>193</Volume>
<Issue>6</Issue>
<PubDate><Year>2014</Year>
<Month>Sep</Month>
<Day>15</Day>
</PubDate>
</JournalIssue>
<Title>Journal of immunology (Baltimore, Md. : 1950)</Title>
<ISOAbbreviation>J. Immunol.</ISOAbbreviation>
</Journal>
<ArticleTitle>SARS-coronavirus open reading frame-9b suppresses innate immunity by targeting mitochondria and the MAVS/TRAF3/TRAF6 signalosome.</ArticleTitle>
<Pagination><MedlinePgn>3080-9</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.4049/jimmunol.1303196</ELocationID>
<Abstract><AbstractText>Coronaviruses (CoV) have recently emerged as potentially serious pathogens that can cause significant human morbidity and death. The severe acute respiratory syndrome (SARS)-CoV was identified as the etiologic agent of the 2002-2003 international SARS outbreak. Yet, how SARS evades innate immune responses to cause human disease remains poorly understood. In this study, we show that a protein encoded by SARS-CoV designated as open reading frame-9b (ORF-9b) localizes to mitochondria and causes mitochondrial elongation by triggering ubiquitination and proteasomal degradation of dynamin-like protein 1, a host protein involved in mitochondrial fission. Also, acting on mitochondria, ORF-9b targets the mitochondrial-associated adaptor molecule MAVS signalosome by usurping PCBP2 and the HECT domain E3 ligase AIP4 to trigger the degradation of MAVS, TRAF3, and TRAF 6. This severely limits host cell IFN responses. Reducing either PCBP2 or AIP4 expression substantially reversed the ORF-9b-mediated reduction of MAVS and the suppression of antiviral transcriptional responses. Finally, transient ORF-9b expression led to a strong induction of autophagy in cells. The induction of autophagy depended upon ATG5, a critical autophagy regulator, but the inhibition of MAVS signaling did not. These results indicate that SARS-CoV ORF-9b manipulates host cell mitochondria and mitochondrial function to help evade host innate immunity. This study has uncovered an important clue to the pathogenesis of SARS-CoV infection and illustrates the havoc that a small ORF can cause in cells. </AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Shi</LastName>
<ForeName>Chong-Shan</ForeName>
<Initials>CS</Initials>
<AffiliationInfo><Affiliation>B Cell Molecular Immunology Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892;</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Qi</LastName>
<ForeName>Hai-Yan</ForeName>
<Initials>HY</Initials>
<AffiliationInfo><Affiliation>Critical Care Medicine Department, National Institutes of Health, Bethesda, MD 20892; and.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Boularan</LastName>
<ForeName>Cedric</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>B Cell Molecular Immunology Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892;</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Huang</LastName>
<ForeName>Ning-Na</ForeName>
<Initials>NN</Initials>
<AffiliationInfo><Affiliation>B Cell Molecular Immunology Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892;</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Abu-Asab</LastName>
<ForeName>Mones</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Immunopathology Section, National Eye Institute, National Institutes of Health, Bethesda, MD 20892.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Shelhamer</LastName>
<ForeName>James H</ForeName>
<Initials>JH</Initials>
<AffiliationInfo><Affiliation>Critical Care Medicine Department, National Institutes of Health, Bethesda, MD 20892; and.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kehrl</LastName>
<ForeName>John H</ForeName>
<Initials>JH</Initials>
<AffiliationInfo><Affiliation>B Cell Molecular Immunology Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892; jkehrl@niaid.nih.gov.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>ZIA AI000739-14</GrantID>
<Agency>Intramural NIH HHS</Agency>
<Country>United States</Country>
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<Month>08</Month>
<Day>18</Day>
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<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>J Immunol</MedlineTA>
<NlmUniqueID>2985117R</NlmUniqueID>
<ISSNLinking>0022-1767</ISSNLinking>
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<Chemical><RegistryNumber>0</RegistryNumber>
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<Chemical><RegistryNumber>0</RegistryNumber>
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<Chemical><RegistryNumber>0</RegistryNumber>
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<NameOfSubstance UI="D048008">TNF Receptor-Associated Factor 3</NameOfSubstance>
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<Chemical><RegistryNumber>147336-22-9</RegistryNumber>
<NameOfSubstance UI="D049452">Green Fluorescent Proteins</NameOfSubstance>
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<Chemical><RegistryNumber>EC 2.3.2.26</RegistryNumber>
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<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D001343" MajorTopicYN="N">Autophagy</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
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<MeshHeading><DescriptorName UI="D000071187" MajorTopicYN="N">Autophagy-Related Protein 5</DescriptorName>
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<MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName>
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<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
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<MeshHeading><DescriptorName UI="D057809" MajorTopicYN="N">HEK293 Cells</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D057131" MajorTopicYN="N">Immune Evasion</DescriptorName>
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<QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName>
<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
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<MeshHeading><DescriptorName UI="D016366" MajorTopicYN="N">Open Reading Frames</DescriptorName>
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<ArticleIdList><ArticleId IdType="pubmed">25135833</ArticleId>
<ArticleId IdType="pii">jimmunol.1303196</ArticleId>
<ArticleId IdType="doi">10.4049/jimmunol.1303196</ArticleId>
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</ArticleIdList>
<ReferenceList><Reference><Citation>Cell. 2013 Apr 11;153(2):348-61</Citation>
<ArticleIdList><ArticleId IdType="pubmed">23582325</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>PLoS Pathog. 2013 Mar;9(3):e1003285</Citation>
<ArticleIdList><ArticleId IdType="pubmed">23555273</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>BMC Neurosci. 2013;14:86</Citation>
<ArticleIdList><ArticleId IdType="pubmed">23937156</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Mol Biol. 2013 Dec 13;425(24):5009-19</Citation>
<ArticleIdList><ArticleId IdType="pubmed">24120683</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Antiviral Res. 2013 Oct;100(1):286-95</Citation>
<ArticleIdList><ArticleId IdType="pubmed">24012996</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Mol Biol Cell. 2008 May;19(5):1903-11</Citation>
<ArticleIdList><ArticleId IdType="pubmed">18287522</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Lancet. 2003 Apr 19;361(9366):1319-25</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12711465</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>Science. 2003 May 30;300(5624):1394-9</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12730500</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Science. 2003 May 30;300(5624):1399-404</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12730501</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nat Rev Microbiol. 2003 Dec;1(3):209-18</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15035025</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Expert Opin Biol Ther. 2004 Jun;4(6):827-36</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15174965</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nat Med. 2004 Dec;10(12 Suppl):S88-97</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15577937</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Infect Dis. 2005 Jan 15;191(2):193-7</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15609228</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Virol. 2005 Feb;79(4):2079-86</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15681410</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Microbes Infect. 2005 May;7(5-6):882-9</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15878679</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Exp Med. 2005 Aug 1;202(3):415-24</Citation>
<ArticleIdList><ArticleId IdType="pubmed">16043521</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cell. 2005 Sep 9;122(5):669-82</Citation>
<ArticleIdList><ArticleId IdType="pubmed">16125763</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Mod Pathol. 2005 Nov;18(11):1432-9</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15920543</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Proc Natl Acad Sci U S A. 2005 Dec 6;102(49):17717-22</Citation>
<ArticleIdList><ArticleId IdType="pubmed">16301520</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Structure. 2006 Jul;14(7):1157-65</Citation>
<ArticleIdList><ArticleId IdType="pubmed">16843897</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Biochem. 2007 Feb;141(2):137-45</Citation>
<ArticleIdList><ArticleId IdType="pubmed">17190786</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Virus Res. 2007 Jul;127(1):116-21</Citation>
<ArticleIdList><ArticleId IdType="pubmed">17448558</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Proc Natl Acad Sci U S A. 2007 Aug 28;104(35):14050-5</Citation>
<ArticleIdList><ArticleId IdType="pubmed">17709747</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Proc Natl Acad Sci U S A. 2009 Feb 24;106(8):2770-5</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19196953</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>PLoS Pathog. 2009 Nov;5(11):e1000650</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19893624</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nat Immunol. 2009 Dec;10(12):1300-8</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19881509</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>EMBO Rep. 2010 Feb;11(2):133-8</Citation>
<ArticleIdList><ArticleId IdType="pubmed">20019757</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Sci Signal. 2010;3(123):ra42</Citation>
<ArticleIdList><ArticleId IdType="pubmed">20501938</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Immunol. 2010 Jul 15;185(2):1158-68</Citation>
<ArticleIdList><ArticleId IdType="pubmed">20554965</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Biol Chem. 2011 Apr 1;286(13):11649-58</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21292769</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nat Cell Biol. 2011 May;13(5):589-98</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21478857</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>PLoS One. 2011;6(5):e19436</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21637748</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Proc Natl Acad Sci U S A. 2011 Jun 21;108(25):10190-5</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21646527</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Proc Natl Acad Sci U S A. 2011 Aug 30;108(35):14590-5</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21844353</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nat Immunol. 2012 Mar;13(3):255-63</Citation>
<ArticleIdList><ArticleId IdType="pubmed">22286270</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>New Microbiol. 2012 Jan;35(1):1-16</Citation>
<ArticleIdList><ArticleId IdType="pubmed">22378548</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Science. 2012 Aug 31;337(6098):1062-5</Citation>
<ArticleIdList><ArticleId IdType="pubmed">22936770</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nature. 2012 Oct 4;490(7418):20</Citation>
<ArticleIdList><ArticleId IdType="pubmed">23038444</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Virol. 2012 Dec;86(23):13049-61</Citation>
<ArticleIdList><ArticleId IdType="pubmed">23015697</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>N Engl J Med. 2012 Nov 8;367(19):1814-20</Citation>
<ArticleIdList><ArticleId IdType="pubmed">23075143</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Viruses. 2012 Nov;4(11):2902-23</Citation>
<ArticleIdList><ArticleId IdType="pubmed">23202509</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Viruses. 2012 Dec;4(12):3440-51</Citation>
<ArticleIdList><ArticleId IdType="pubmed">23202545</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>PLoS One. 2013;8(1):e52909</Citation>
<ArticleIdList><ArticleId IdType="pubmed">23320079</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Biochim Biophys Acta. 2013 May;1833(5):1256-68</Citation>
<ArticleIdList><ArticleId IdType="pubmed">23434681</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>PLoS Pathog. 2013 Mar;9(3):e1003231</Citation>
<ArticleIdList><ArticleId IdType="pubmed">23555247</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cell Res. 2013 Aug;23(8):1025-42</Citation>
<ArticleIdList><ArticleId IdType="pubmed">23877405</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
</PubmedData>
</pubmed>
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