| pubmed-article:21703540 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:21703540 | lifeskim:mentions | umls-concept:C0021311 | lld:lifeskim |
| pubmed-article:21703540 | lifeskim:mentions | umls-concept:C0033684 | lld:lifeskim |
| pubmed-article:21703540 | lifeskim:mentions | umls-concept:C1155266 | lld:lifeskim |
| pubmed-article:21703540 | lifeskim:mentions | umls-concept:C1826442 | lld:lifeskim |
| pubmed-article:21703540 | lifeskim:mentions | umls-concept:C0086982 | lld:lifeskim |
| pubmed-article:21703540 | lifeskim:mentions | umls-concept:C0599946 | lld:lifeskim |
| pubmed-article:21703540 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:21703540 | pubmed:dateCreated | 2011-6-27 | lld:pubmed |
| pubmed-article:21703540 | pubmed:abstractText | The nucleotide-binding domain and leucine-rich-repeat-containing (NLR) proteins regulate innate immunity. Although the positive regulatory impact of NLRs is clear, their inhibitory roles are not well defined. We showed that Nlrx1(-/-) mice exhibited increased expression of antiviral signaling molecules IFN-?, STAT2, OAS1, and IL-6 after influenza virus infection. Consistent with increased inflammation, Nlrx1(-/-) mice exhibited marked morbidity and histopathology. Infection of these mice with an influenza strain that carries a mutated NS-1 protein, which normally prevents IFN induction by interaction with RNA and the intracellular RNA sensor RIG-I, further exacerbated IL-6 and type I IFN signaling. NLRX1 also weakened cytokine responses to the 2009 H1N1 pandemic influenza virus in human cells. Mechanistically, Nlrx1 deletion led to constitutive interaction of MAVS and RIG-I. Additionally, an inhibitory function is identified for NLRX1 during LPS activation of macrophages where the MAVS-RIG-I pathway was not involved. NLRX1 interacts with TRAF6 and inhibits NF-?B activation. Thus, NLRX1 functions as a checkpoint of overzealous inflammation. | lld:pubmed |
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| pubmed-article:21703540 | pubmed:language | eng | lld:pubmed |
| pubmed-article:21703540 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21703540 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:21703540 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:21703540 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:21703540 | pubmed:issn | 1097-4180 | lld:pubmed |
| pubmed-article:21703540 | pubmed:author | pubmed-author:YuLeiL | lld:pubmed |
| pubmed-article:21703540 | pubmed:author | pubmed-author:PicklesRaymon... | lld:pubmed |
| pubmed-article:21703540 | pubmed:author | pubmed-author:SambharaSurya... | lld:pubmed |
| pubmed-article:21703540 | pubmed:author | pubmed-author:GrisDenisD | lld:pubmed |
| pubmed-article:21703540 | pubmed:author | pubmed-author:DavisBeckley... | lld:pubmed |
| pubmed-article:21703540 | pubmed:author | pubmed-author:RanjanPriyaP | lld:pubmed |
| pubmed-article:21703540 | pubmed:author | pubmed-author:RoneyKelly... | lld:pubmed |
| pubmed-article:21703540 | pubmed:author | pubmed-author:TingJenny P... | lld:pubmed |
| pubmed-article:21703540 | pubmed:author | pubmed-author:AllenIrving... | lld:pubmed |
| pubmed-article:21703540 | pubmed:author | pubmed-author:MooreChris... | lld:pubmed |
| pubmed-article:21703540 | pubmed:author | pubmed-author:ZimmermannAlb... | lld:pubmed |
| pubmed-article:21703540 | pubmed:author | pubmed-author:SchneiderMoni... | lld:pubmed |
| pubmed-article:21703540 | pubmed:author | pubmed-author:ScullMargaret... | lld:pubmed |
| pubmed-article:21703540 | pubmed:author | pubmed-author:MonroeKathryn... | lld:pubmed |
| pubmed-article:21703540 | pubmed:author | pubmed-author:BowzardJohn... | lld:pubmed |
| pubmed-article:21703540 | pubmed:copyrightInfo | Copyright © 2011 Elsevier Inc. All rights reserved. | lld:pubmed |
| pubmed-article:21703540 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:21703540 | pubmed:day | 24 | lld:pubmed |
| pubmed-article:21703540 | pubmed:volume | 34 | lld:pubmed |
| pubmed-article:21703540 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:21703540 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:21703540 | pubmed:pagination | 854-65 | lld:pubmed |
| pubmed-article:21703540 | pubmed:dateRevised | 2011-9-6 | lld:pubmed |
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| pubmed-article:21703540 | pubmed:year | 2011 | lld:pubmed |
| pubmed-article:21703540 | pubmed:articleTitle | NLRX1 protein attenuates inflammatory responses to infection by interfering with the RIG-I-MAVS and TRAF6-NF-?B signaling pathways. | lld:pubmed |
| pubmed-article:21703540 | pubmed:affiliation | The Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA. | lld:pubmed |
| pubmed-article:21703540 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:21703540 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
| entrez-gene:270151 | entrezgene:pubmed | pubmed-article:21703540 | lld:entrezgene |
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