MAVS-mediated apoptosis and its inhibition by viral proteins.
Identifieur interne : 001841 ( PubMed/Checkpoint ); précédent : 001840; suivant : 001842MAVS-mediated apoptosis and its inhibition by viral proteins.
Auteurs : Yu Lei [États-Unis] ; Chris B. Moore ; Rachael M. Liesman ; Brian P. O'Connor ; Daniel T. Bergstralh ; Zhijian J. Chen ; Raymond J. Pickles ; Jenny P-Y TingSource :
- PloS one [ 1932-6203 ] ; 2009.
Descripteurs français
- KwdFr :
- Animaux, Apoptose (immunologie), Apoptose (physiologie), Caspases (métabolisme), Cellules cultivées, Facteur de transcription NF-kappa B (métabolisme), Facteur-3 de régulation d'interféron (antagonistes et inhibiteurs), Facteur-3 de régulation d'interféron (génétique), Humains, Interactions hôte-pathogène (immunologie), Interactions hôte-pathogène (physiologie), Interféron de type I (biosynthèse), Lignée cellulaire, Mitochondries (métabolisme), Modèles biologiques, Petit ARN interférent (génétique), Protéines adaptatrices de la transduction du signal (), Protéines adaptatrices de la transduction du signal (déficit), Protéines adaptatrices de la transduction du signal (génétique), Protéines adaptatrices de la transduction du signal (physiologie), Protéines virales (physiologie), Protéines virales non structurales (physiologie), RNA replicase (physiologie), Souris, Souris knockout, Structure tertiaire des protéines, Séquence nucléotidique, Virus Sendai (pathogénicité).
- MESH :
- antagonistes et inhibiteurs : Facteur-3 de régulation d'interféron.
- biosynthèse : Interféron de type I.
- déficit : Protéines adaptatrices de la transduction du signal.
- génétique : Facteur-3 de régulation d'interféron, Petit ARN interférent, Protéines adaptatrices de la transduction du signal.
- immunologie : Apoptose, Interactions hôte-pathogène.
- métabolisme : Caspases, Facteur de transcription NF-kappa B, Mitochondries.
- pathogénicité : Virus Sendai.
- physiologie : Apoptose, Interactions hôte-pathogène, Protéines adaptatrices de la transduction du signal, Protéines virales, Protéines virales non structurales, RNA replicase.
- Animaux, Cellules cultivées, Humains, Lignée cellulaire, Modèles biologiques, Protéines adaptatrices de la transduction du signal, Souris, Souris knockout, Structure tertiaire des protéines, Séquence nucléotidique.
English descriptors
- KwdEn :
- Adaptor Proteins, Signal Transducing (chemistry), Adaptor Proteins, Signal Transducing (deficiency), Adaptor Proteins, Signal Transducing (genetics), Adaptor Proteins, Signal Transducing (physiology), Animals, Apoptosis (immunology), Apoptosis (physiology), Base Sequence, Caspases (metabolism), Cell Line, Cells, Cultured, Host-Pathogen Interactions (immunology), Host-Pathogen Interactions (physiology), Humans, Interferon Regulatory Factor-3 (antagonists & inhibitors), Interferon Regulatory Factor-3 (genetics), Interferon Type I (biosynthesis), Mice, Mice, Knockout, Mitochondria (metabolism), Models, Biological, NF-kappa B (metabolism), Protein Structure, Tertiary, RNA Replicase (physiology), RNA, Small Interfering (genetics), Sendai virus (pathogenicity), Viral Nonstructural Proteins (physiology), Viral Proteins (physiology).
- MESH :
- chemical , antagonists & inhibitors : Interferon Regulatory Factor-3.
- chemical , biosynthesis : Interferon Type I.
- chemical , chemistry : Adaptor Proteins, Signal Transducing.
- chemical , deficiency : Adaptor Proteins, Signal Transducing.
- chemical , genetics : Adaptor Proteins, Signal Transducing, Interferon Regulatory Factor-3, RNA, Small Interfering.
- chemical , metabolism : Caspases, NF-kappa B.
- chemical , physiology : Adaptor Proteins, Signal Transducing, RNA Replicase, Viral Nonstructural Proteins, Viral Proteins.
- immunology : Apoptosis, Host-Pathogen Interactions.
- metabolism : Mitochondria.
- pathogenicity : Sendai virus.
- physiology : Apoptosis, Host-Pathogen Interactions.
- Animals, Base Sequence, Cell Line, Cells, Cultured, Humans, Mice, Mice, Knockout, Models, Biological, Protein Structure, Tertiary.
Abstract
Host responses to viral infection include both immune activation and programmed cell death. The mitochondrial antiviral signaling adaptor, MAVS (IPS-1, VISA or Cardif) is critical for host defenses to viral infection by inducing type-1 interferons (IFN-I), however its role in virus-induced apoptotic responses has not been elucidated.
DOI: 10.1371/journal.pone.0005466
PubMed: 19404494
Affiliations:
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pubmed:19404494Le document en format XML
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Cultured</term><term>Humans</term><term>Mice</term><term>Mice, Knockout</term><term>Models, Biological</term><term>Protein Structure, Tertiary</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Cellules cultivées</term><term>Humains</term><term>Lignée cellulaire</term><term>Modèles biologiques</term><term>Protéines adaptatrices de la transduction du signal</term><term>Souris</term><term>Souris knockout</term><term>Structure tertiaire des protéines</term><term>Séquence nucléotidique</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Host responses to viral infection include both immune activation and programmed cell death. The mitochondrial antiviral signaling adaptor, MAVS (IPS-1, VISA or Cardif) is critical for host defenses to viral infection by inducing type-1 interferons (IFN-I), however its role in virus-induced apoptotic responses has not been elucidated.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">19404494</PMID><DateCompleted><Year>2009</Year><Month>06</Month><Day>17</Day></DateCompleted><DateRevised><Year>2020</Year><Month>03</Month><Day>26</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1932-6203</ISSN><JournalIssue CitedMedium="Internet"><Volume>4</Volume><Issue>5</Issue><PubDate><Year>2009</Year></PubDate></JournalIssue><Title>PloS one</Title><ISOAbbreviation>PLoS ONE</ISOAbbreviation></Journal><ArticleTitle>MAVS-mediated apoptosis and its inhibition by viral proteins.</ArticleTitle><Pagination><MedlinePgn>e5466</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pone.0005466</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Host responses to viral infection include both immune activation and programmed cell death. The mitochondrial antiviral signaling adaptor, MAVS (IPS-1, VISA or Cardif) is critical for host defenses to viral infection by inducing type-1 interferons (IFN-I), however its role in virus-induced apoptotic responses has not been elucidated.</AbstractText><AbstractText Label="PRINCIPAL FINDINGS" NlmCategory="RESULTS">We show that MAVS causes apoptosis independent of its function in initiating IFN-I production. MAVS-induced cell death requires mitochondrial localization, is caspase dependent, and displays hallmarks of apoptosis. Furthermore, MAVS(-/-) fibroblasts are resistant to Sendai virus-induced apoptosis. A functional screen identifies the hepatitis C virus NS3/4A and the Severe Acute Respiratory Syndrome coronavirus (SARS-CoV) nonstructural protein (NSP15) as inhibitors of MAVS-induced apoptosis, possibly as a method of immune evasion.</AbstractText><AbstractText Label="SIGNIFICANCE" NlmCategory="CONCLUSIONS">This study describes a novel role for MAVS in controlling viral infections through the induction of apoptosis, and identifies viral proteins which inhibit this host response.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lei</LastName><ForeName>Yu</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, North Carolina, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Moore</LastName><ForeName>Chris B</ForeName><Initials>CB</Initials></Author><Author ValidYN="Y"><LastName>Liesman</LastName><ForeName>Rachael M</ForeName><Initials>RM</Initials></Author><Author ValidYN="Y"><LastName>O'Connor</LastName><ForeName>Brian P</ForeName><Initials>BP</Initials></Author><Author ValidYN="Y"><LastName>Bergstralh</LastName><ForeName>Daniel T</ForeName><Initials>DT</Initials></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Zhijian J</ForeName><Initials>ZJ</Initials></Author><Author ValidYN="Y"><LastName>Pickles</LastName><ForeName>Raymond J</ForeName><Initials>RJ</Initials></Author><Author ValidYN="Y"><LastName>Ting</LastName><ForeName>Jenny P-Y</ForeName><Initials>JP</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2009</Year><Month>03</Month><Day>07</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>PLoS One</MedlineTA><NlmUniqueID>101285081</NlmUniqueID><ISSNLinking>1932-6203</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D048868">Adaptor Proteins, Signal Transducing</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C512612">IPS-1 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C494232">IRF3 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D050838">Interferon Regulatory Factor-3</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007370">Interferon Type I</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016328">NF-kappa B</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D034741">RNA, Small Interfering</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C505371">VISA protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017361">Viral Nonstructural Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014764">Viral Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.7.48</RegistryNumber><NameOfSubstance UI="D012324">RNA Replicase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.1.-</RegistryNumber><NameOfSubstance UI="C000657925">nidoviral uridylate-specific endoribonuclease</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.22.-</RegistryNumber><NameOfSubstance UI="D020169">Caspases</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D048868" MajorTopicYN="N">Adaptor Proteins, Signal Transducing</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000172" MajorTopicYN="N">deficiency</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001483" MajorTopicYN="N">Base Sequence</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020169" MajorTopicYN="N">Caspases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D054884" MajorTopicYN="N">Host-Pathogen Interactions</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D050838" MajorTopicYN="N">Interferon Regulatory Factor-3</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007370" MajorTopicYN="N">Interferon Type I</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="N">biosynthesis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008928" MajorTopicYN="N">Mitochondria</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008954" MajorTopicYN="N">Models, Biological</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016328" MajorTopicYN="N">NF-kappa B</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017434" MajorTopicYN="N">Protein Structure, Tertiary</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012324" MajorTopicYN="N">RNA Replicase</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D034741" MajorTopicYN="N">RNA, Small Interfering</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D029082" MajorTopicYN="N">Sendai virus</DescriptorName><QualifierName UI="Q000472" MajorTopicYN="N">pathogenicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017361" MajorTopicYN="N">Viral Nonstructural Proteins</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014764" MajorTopicYN="N">Viral Proteins</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2008</Year><Month>12</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2009</Year><Month>04</Month><Day>01</Day></PubMedPubDate><PubMedPubDate 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