Source:http://linkedlifedata.com/resource/pubmed/id/17475874
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
10
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pubmed:dateCreated |
2007-5-3
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pubmed:abstractText |
The DExD/H box RNA helicase retinoic acid-inducible gene I (RIG-I) and the melanoma differentiation-associated gene 5 (MDA5) are key intracellular receptors that recognize virus infection to produce type I IFN. A third helicase gene, Lgp2, is homologous to Rig-I and Mda5 but lacks a caspase activation and recruitment domain. We generated Lgp2-deficient mice and report that the loss of this gene greatly sensitizes cells to cytosolic polyinosinic/polycytidylic acid-mediated induction of type I IFN. However, negative feedback inhibition of IFN-beta transcription was found to be normal in the absence of LGP2, indicating that LGP2 is not the primary negative regulator of type I IFN production. Our data further indicate that Lgp2-/- mice exhibited resistance to lethal vesicular stomatitis virus infection, a virus whose replicative RNA intermediates are recognized specifically by RIG-I rather than by MDA5 to trigger the production of type I IFN. However, mice lacking LGP2 were observed to exhibit a defect in type I IFN production in response to infection by the encephalomyocarditis virus, the replication of which activates MDA5-dependent innate immune responses. Collectively, our data indicate a disparate regulatory role for LGP2 in the triggering of innate immune signaling pathways following RNA virus infection.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/DEAD-box RNA Helicases,
http://linkedlifedata.com/resource/pubmed/chemical/Ddx58 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Ifih1protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Nerve Tissue Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Robo3 protein, mouse
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
178
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
6444-55
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:17475874-Animals,
pubmed-meshheading:17475874-Cardiovirus Infections,
pubmed-meshheading:17475874-Cells, Cultured,
pubmed-meshheading:17475874-DEAD-box RNA Helicases,
pubmed-meshheading:17475874-Encephalomyocarditis virus,
pubmed-meshheading:17475874-Female,
pubmed-meshheading:17475874-Immunity, Innate,
pubmed-meshheading:17475874-Male,
pubmed-meshheading:17475874-Membrane Proteins,
pubmed-meshheading:17475874-Mice,
pubmed-meshheading:17475874-Mice, Inbred C57BL,
pubmed-meshheading:17475874-Mice, Transgenic,
pubmed-meshheading:17475874-Nerve Tissue Proteins,
pubmed-meshheading:17475874-Rhabdoviridae Infections,
pubmed-meshheading:17475874-Signal Transduction,
pubmed-meshheading:17475874-Vesicular stomatitis Indiana virus
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pubmed:year |
2007
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pubmed:articleTitle |
Loss of DExD/H box RNA helicase LGP2 manifests disparate antiviral responses.
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pubmed:affiliation |
Department of Microbiology and Immunology and Sylvester Comprehensive Cancer Center, University of Miami School of Medicine, Miami, FL 33136, USA.
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pubmed:publicationType |
Journal Article
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