| Requirement of NOX2 and reactive oxygen species for efficient RIG-I-mediated antiviral response through regulation of MAVS expression. | |
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MedLine Citation:
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PMID: 20532218 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The innate immune response is essential to the host defense against viruses, through restriction of virus replication and coordination of the adaptive immune response. Induction of antiviral genes is a tightly regulated process initiated mainly through sensing of invading virus nucleic acids in the cytoplasm by RIG-I like helicases, RIG-I or Mda5, which transmit the signal through a common mitochondria-associated adaptor, MAVS. Although major breakthroughs have recently been made, much remains unknown about the mechanisms that translate virus recognition into antiviral genes expression. Beside the reputed detrimental role, reactive oxygen species (ROS) act as modulators of cellular signaling and gene regulation. NADPH oxidase (NOX) enzymes are a main source of deliberate cellular ROS production. Here, we found that NOX2 and ROS are required for the host cell to trigger an efficient RIG-I-mediated IRF-3 activation and downstream antiviral IFNbeta and IFIT1 gene expression. Additionally, we provide evidence that NOX2 is critical for the expression of the central mitochondria-associated adaptor MAVS. Taken together these data reveal a new facet to the regulation of the innate host defense against viruses through the identification of an unrecognized role of NOX2 and ROS. |
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Authors:
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Anton Soucy-Faulkner; Espérance Mukawera; Karin Fink; Alexis Martel; Loubna Jouan; Yves Nzengue; Daniel Lamarre; Christine Vande Velde; Nathalie Grandvaux |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-06-03 |
Journal Detail:
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Title: PLoS pathogens Volume: 6 ISSN: 1553-7374 ISO Abbreviation: PLoS Pathog. Publication Date: 2010 |
Date Detail:
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Created Date: 2010-06-10 Completed Date: 2010-10-27 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 101238921 Medline TA: PLoS Pathog Country: United States |
Other Details:
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Languages: eng Pagination: e1000930 Citation Subset: IM |
Affiliation:
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CRCHUM - Centre Hospitalier de l'Université de Montréal, Montréal, Québec, Canada. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adaptor Proteins, Signal Transducing
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genetics*,
metabolism Blotting, Western Bronchi / cytology, immunology*, metabolism Carrier Proteins / genetics, metabolism Cells, Cultured DEAD-box RNA Helicases / genetics, metabolism* Gene Expression Regulation* Humans Immunity, Innate Interferon Regulatory Factor-3 / genetics, metabolism Interleukin-6 / genetics, metabolism Luciferases / metabolism Lung Neoplasms / immunology*, metabolism, virology Membrane Glycoproteins / genetics, metabolism* NADPH Oxidase / genetics, metabolism* RNA, Messenger / genetics Reactive Oxygen Species / metabolism* Respirovirus Infections / immunology, metabolism, virology Reverse Transcriptase Polymerase Chain Reaction Sendai virus / physiology Signal Transduction |
| Grant Support | |
ID/Acronym/Agency:
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MOP#89807//Canadian Institutes of Health Research |
| Chemical | |
Reg. No./Substance:
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0/Adaptor Proteins, Signal Transducing; 0/CYBB protein, human; 0/Carrier Proteins; 0/IFIT1 protein, human; 0/Interferon Regulatory Factor-3; 0/Interleukin-6; 0/Membrane Glycoproteins; 0/RNA, Messenger; 0/Reactive Oxygen Species; 0/VISA protein, human; EC 1.13.12.-/Luciferases; EC 1.6.3.1/NADPH Oxidase; EC 3.6.1.-/DDX58 protein, human; EC 3.6.1.-/DEAD-box RNA Helicases |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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