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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
7
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pubmed:dateCreated |
2009-6-18
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pubmed:abstractText |
E3 ubiquitin ligases are important in both innate and adaptive immunity. Here we report that Nrdp1, an E3 ubiquitin ligase, inhibited the production of proinflammatory cytokines but increased interferon-beta production in Toll-like receptor-triggered macrophages by suppressing adaptor MyD88-dependent activation of transcription factors NF-kappaB and AP-1 while promoting activation of the kinase TBK1 and transcription factor IRF3. Nrdp1 directly bound and polyubiquitinated MyD88 and TBK1, which led to degradation of MyD88 and activation of TBK1. Knockdown of Nrdp1 inhibited the degradation of MyD88 and the activation of TBK1 and IRF3. Nrdp1-transgenic mice showed resistance to lipopolysaccharide-induced endotoxin shock and to infection with vesicular stomatitis virus. Our data suggest that Nrdp1 functions as both an adaptor protein and an E3 unbiquitin ligase to regulate TLR responses in different ways.
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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/Carrier Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon Type I,
http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/Myd88 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Myeloid Differentiation Factor 88,
http://linkedlifedata.com/resource/pubmed/chemical/Protein-Serine-Threonine Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Rnf41 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Tbk1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Toll-Like Receptors,
http://linkedlifedata.com/resource/pubmed/chemical/Ubiquitin-Protein Ligases
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
1529-2916
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:volume |
10
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
744-52
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pubmed:meshHeading |
pubmed-meshheading:19483718-Animals,
pubmed-meshheading:19483718-Carrier Proteins,
pubmed-meshheading:19483718-Cell Line,
pubmed-meshheading:19483718-Cells, Cultured,
pubmed-meshheading:19483718-Female,
pubmed-meshheading:19483718-Host-Pathogen Interactions,
pubmed-meshheading:19483718-Humans,
pubmed-meshheading:19483718-Immunoblotting,
pubmed-meshheading:19483718-Interferon Type I,
pubmed-meshheading:19483718-Lipopolysaccharides,
pubmed-meshheading:19483718-Macrophages,
pubmed-meshheading:19483718-Macrophages, Peritoneal,
pubmed-meshheading:19483718-Male,
pubmed-meshheading:19483718-Mice,
pubmed-meshheading:19483718-Mice, Inbred C57BL,
pubmed-meshheading:19483718-Mice, Transgenic,
pubmed-meshheading:19483718-Myeloid Differentiation Factor 88,
pubmed-meshheading:19483718-Protein Binding,
pubmed-meshheading:19483718-Protein-Serine-Threonine Kinases,
pubmed-meshheading:19483718-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:19483718-Rhabdoviridae Infections,
pubmed-meshheading:19483718-Sepsis,
pubmed-meshheading:19483718-Toll-Like Receptors,
pubmed-meshheading:19483718-Ubiquitin-Protein Ligases,
pubmed-meshheading:19483718-Vesiculovirus
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pubmed:year |
2009
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pubmed:articleTitle |
The E3 ubiquitin ligase Nrdp1 'preferentially' promotes TLR-mediated production of type I interferon.
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pubmed:affiliation |
National Key Laboratory of Medical Immunology & Institute of Immunology, Second Military Medical University, Shanghai, China.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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