| pubmed-article:20434986 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20434986 | lifeskim:mentions | umls-concept:C0021743 | lld:lifeskim |
| pubmed-article:20434986 | lifeskim:mentions | umls-concept:C0079904 | lld:lifeskim |
| pubmed-article:20434986 | lifeskim:mentions | umls-concept:C1826434 | lld:lifeskim |
| pubmed-article:20434986 | lifeskim:mentions | umls-concept:C0086982 | lld:lifeskim |
| pubmed-article:20434986 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:20434986 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:20434986 | pubmed:dateCreated | 2010-5-3 | lld:pubmed |
| pubmed-article:20434986 | pubmed:abstractText | Stringent control of the NF-kappaB and type I interferon signaling pathways is critical to effective host immune responses, yet the molecular mechanisms that negatively regulate these pathways are poorly understood. Here, we show that NLRC5, a member of the highly conserved NOD-like protein family, can inhibit the IKK complex and RIG-I/MDA5 function. NLRC5 inhibited NF-kappaB-dependent responses by interacting with IKKalpha and IKKbeta and blocking their phosphorylation. It also interacted with RIG-I and MDA5, but not with MAVS, to inhibit RLR-mediated type I interferon responses. Consistent with these observations, NLRC5-specific siRNA knockdown not only enhanced the activation of NF-kappaB and its responsive genes, TNF-alpha and IL-6, but also promoted type I interferon signaling and antiviral immunity. Our findings identify NLRC5 as a negative regulator that blocks two central components of the NF-kappaB and type I interferon signaling pathways and suggest an important role for NLRC5 in homeostatic control of innate immunity. | lld:pubmed |
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| pubmed-article:20434986 | pubmed:language | eng | lld:pubmed |
| pubmed-article:20434986 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20434986 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:20434986 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:20434986 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:20434986 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:20434986 | pubmed:issn | 1097-4172 | lld:pubmed |
| pubmed-article:20434986 | pubmed:author | pubmed-author:WangRong-FuRF | lld:pubmed |
| pubmed-article:20434986 | pubmed:author | pubmed-author:WangHelen YHY | lld:pubmed |
| pubmed-article:20434986 | pubmed:author | pubmed-author:HongJunJ | lld:pubmed |
| pubmed-article:20434986 | pubmed:author | pubmed-author:ZhuLiangL | lld:pubmed |
| pubmed-article:20434986 | pubmed:author | pubmed-author:ShenPingpingP | lld:pubmed |
| pubmed-article:20434986 | pubmed:author | pubmed-author:ZhengShuS | lld:pubmed |
| pubmed-article:20434986 | pubmed:author | pubmed-author:ChenZhijian... | lld:pubmed |
| pubmed-article:20434986 | pubmed:author | pubmed-author:MAYE LEL | lld:pubmed |
| pubmed-article:20434986 | pubmed:author | pubmed-author:JiJiabingJ | lld:pubmed |
| pubmed-article:20434986 | pubmed:author | pubmed-author:XiaXiaojunX | lld:pubmed |
| pubmed-article:20434986 | pubmed:author | pubmed-author:LegrasXavierX | lld:pubmed |
| pubmed-article:20434986 | pubmed:copyrightInfo | 2010 Elsevier Inc. All rights reserved. | lld:pubmed |
| pubmed-article:20434986 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:20434986 | pubmed:day | 30 | lld:pubmed |
| pubmed-article:20434986 | pubmed:volume | 141 | lld:pubmed |
| pubmed-article:20434986 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:20434986 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:20434986 | pubmed:pagination | 483-96 | lld:pubmed |
| pubmed-article:20434986 | pubmed:dateRevised | 2011-10-4 | lld:pubmed |
| pubmed-article:20434986 | pubmed:meshHeading | pubmed-meshheading:20434986... | lld:pubmed |
| pubmed-article:20434986 | pubmed:meshHeading | pubmed-meshheading:20434986... | lld:pubmed |
| pubmed-article:20434986 | pubmed:meshHeading | pubmed-meshheading:20434986... | lld:pubmed |
