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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1-2
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pubmed:dateCreated |
2004-10-11
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pubmed:abstractText |
Toll-like receptor 3 (TLR3) recognizes dsRNA generated during viral infection and activation of TLR3 results in induction of type I interferons (IFNs) and cellular anti-viral response. TLR3 is associated with a TIR domain-containing adapter protein TRIF, which activates distinct downstream pathways leading to activation of NF-kappaB and ISRE sites in the promoters of type I IFNs. We show here that A20, a NF-kappaB-inducible zinc finger protein that has been demonstrated to be an inhibitor of TNF-induced NF-kappaB activation and a physiological suppressor of inflammatory response, potently inhibited TLR3- and Sendai virus-mediated activation of ISRE and NF-kappaB and IFN-beta promoter in reporter gene assays. A20 also inhibited TRIF-, but not its downstream signaling components TBK1-, IKKbeta-, and IKKepsilon-mediated activation of ISRE and NF-kappaB and IFN-beta promoter. Moreover, A20 interacted with TRIF in co-immunoprecipitation experiments. Finally, expression of A20 could be induced at protein level by Sendai virus infection. These data suggest that A20 targets TRIF to inhibit TLR3-mediated induction of IFN-beta transcription and functions as a feedback negative regulator for TLR3 signaling and cellular anti-viral response.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adaptor Proteins, Vesicular...,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-beta,
http://linkedlifedata.com/resource/pubmed/chemical/Intracellular Signaling Peptides...,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B,
http://linkedlifedata.com/resource/pubmed/chemical/Nuclear Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cell Surface,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Immunologic,
http://linkedlifedata.com/resource/pubmed/chemical/TICAM1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/TLR3 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/TNFAIP3 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Toll-Like Receptor 3,
http://linkedlifedata.com/resource/pubmed/chemical/Toll-Like Receptors
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0014-5793
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pubmed:author |
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pubmed:copyrightInfo |
Copyright 2004 Federation of European Biochemical Societies
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pubmed:issnType |
Print
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pubmed:day |
8
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pubmed:volume |
576
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
86-90
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:15474016-Adaptor Proteins, Vesicular Transport,
pubmed-meshheading:15474016-Blotting, Western,
pubmed-meshheading:15474016-Cell Line,
pubmed-meshheading:15474016-Genes, Reporter,
pubmed-meshheading:15474016-Humans,
pubmed-meshheading:15474016-Interferon-beta,
pubmed-meshheading:15474016-Intracellular Signaling Peptides and Proteins,
pubmed-meshheading:15474016-Membrane Glycoproteins,
pubmed-meshheading:15474016-NF-kappa B,
pubmed-meshheading:15474016-Nuclear Proteins,
pubmed-meshheading:15474016-Precipitin Tests,
pubmed-meshheading:15474016-Promoter Regions, Genetic,
pubmed-meshheading:15474016-Proteins,
pubmed-meshheading:15474016-Receptors, Cell Surface,
pubmed-meshheading:15474016-Receptors, Immunologic,
pubmed-meshheading:15474016-Response Elements,
pubmed-meshheading:15474016-Sendai virus,
pubmed-meshheading:15474016-Toll-Like Receptor 3,
pubmed-meshheading:15474016-Toll-Like Receptors,
pubmed-meshheading:15474016-Virus Activation
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pubmed:year |
2004
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pubmed:articleTitle |
A20 is a potent inhibitor of TLR3- and Sendai virus-induced activation of NF-kappaB and ISRE and IFN-beta promoter.
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pubmed:affiliation |
Department of Cell Biology and Genetics, College of Life Sciences, Peking University, Beijing 100871, China.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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