Abstract
The mitochondria-associated adapter protein MAVS (also called IPS-1, VISA or CARDIF, designated MAVS for reasons of simplicity in our manuscript) relays signals from cytoplasmic sensors of viral RNA to the IRF3 kinase complex and the interferon-beta (IFN-beta) gene. Using siRNA-mediated knock-down in macrophages we show that IFN-beta synthesis in response to transfected, intracellular double-stranded RNA (dsRNA), a pathogen-associated molecular pattern of viruses, is decreased in absence of MAVS. By contrast, the Gram-positive bacterium Listeria monocytogenes targets the IFN-beta gene without detectable MAVS requirement. The data show that MAVS is not a central adapter protein for all cytoplasmic pathogen sensors that stimulate IFN-beta synthesis.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adaptor Proteins, Signal Transducing / genetics
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Adaptor Proteins, Signal Transducing / immunology*
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Animals
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Cell Line
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Cytoplasm / genetics
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Cytoplasm / immunology
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Cytoplasm / metabolism
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Cytoplasm / microbiology
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Interferon-beta / biosynthesis
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Interferon-beta / genetics
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Interferon-beta / immunology*
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Listeria monocytogenes / immunology*
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Listeriosis / genetics
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Listeriosis / immunology*
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Listeriosis / metabolism
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Macrophages / immunology*
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Macrophages / metabolism
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Macrophages / microbiology
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Mice
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RNA, Double-Stranded / genetics
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RNA, Double-Stranded / immunology
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RNA, Small Interfering / genetics
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RNA, Small Interfering / immunology
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Signal Transduction / genetics
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Signal Transduction / immunology*
Substances
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Adaptor Proteins, Signal Transducing
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RNA, Double-Stranded
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RNA, Small Interfering
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VISA protein, mouse
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Interferon-beta