| pubmed-article:17088249 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17088249 | lifeskim:mentions | umls-concept:C1426159 | lld:lifeskim |
| pubmed-article:17088249 | lifeskim:mentions | umls-concept:C1999216 | lld:lifeskim |
| pubmed-article:17088249 | lifeskim:mentions | umls-concept:C1523116 | lld:lifeskim |
| pubmed-article:17088249 | lifeskim:mentions | umls-concept:C0679622 | lld:lifeskim |
| pubmed-article:17088249 | lifeskim:mentions | umls-concept:C0205314 | lld:lifeskim |
| pubmed-article:17088249 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:17088249 | pubmed:dateCreated | 2007-1-1 | lld:pubmed |
| pubmed-article:17088249 | pubmed:abstractText | Recognition of lipopolysaccharide (LPS) by Toll-like receptor (TLR)4 initiates an intracellular signaling pathway leading to the activation of nuclear factor-kappaB (NF-kappaB). Although LPS-induced activation of NF-kappaB is critical to the induction of an efficient immune response, excessive or prolonged signaling from TLR4 can be harmful to the host. Therefore, the NF-kappaB signal transduction pathway demands tight regulation. In the present study, we describe the human protein Listeria INDuced (LIND) as a novel A20-binding inhibitor of NF-kappaB activation (ABIN) that is related to ABIN-1 and -2 and, therefore, is further referred to as ABIN-3. Similar to the other ABINs, ABIN-3 binds to A20 and inhibits NF-kappaB activation induced by tumor necrosis factor, interleukin-1, and 12-O-tetradecanoylphorbol-13-acetate. However, unlike the other ABINs, constitutive expression of ABIN-3 could not be detected in different human cells. Treatment of human monocytic cells with LPS strongly induced ABIN-3 mRNA and protein expression, suggesting a role for ABIN-3 in the LPS/TLR4 pathway. Indeed, ABIN-3 overexpression was found to inhibit NF-kappaB-dependent gene expression in response to LPS/TLR4 at a level downstream of TRAF6 and upstream of IKKbeta. NF-kappaB inhibition was mediated by the ABIN-homology domain 2 and was independent of A20 binding. Moreover, in vivo adenoviral gene transfer of ABIN-3 in mice reduced LPS-induced NF-kappaB activity in the liver, thereby partially protecting mice against LPS/D-(+)-galactosamine-induced mortality. Taken together, these results implicate ABIN-3 as a novel negative feedback regulator of LPS-induced NF-kappaB activation. | lld:pubmed |
| pubmed-article:17088249 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17088249 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17088249 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:17088249 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:17088249 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:17088249 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17088249 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:17088249 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:17088249 | pubmed:author | pubmed-author:CavaillonJean... | lld:pubmed |
| pubmed-article:17088249 | pubmed:author | pubmed-author:BeyaertRudiR | lld:pubmed |
| pubmed-article:17088249 | pubmed:author | pubmed-author:HeyninckKaren... | lld:pubmed |
| pubmed-article:17088249 | pubmed:author | pubmed-author:Adib-ConquyMi... | lld:pubmed |
| pubmed-article:17088249 | pubmed:author | pubmed-author:SandersMatthe... | lld:pubmed |
| pubmed-article:17088249 | pubmed:author | pubmed-author:WullaertAndyA | lld:pubmed |
| pubmed-article:17088249 | pubmed:author | pubmed-author:Van... | lld:pubmed |
| pubmed-article:17088249 | pubmed:author | pubmed-author:KreikeMarjaM | lld:pubmed |
| pubmed-article:17088249 | pubmed:author | pubmed-author:CarpentierIsa... | lld:pubmed |
| pubmed-article:17088249 | pubmed:author | pubmed-author:CornelisSigri... | lld:pubmed |
| pubmed-article:17088249 | pubmed:author | pubmed-author:El... | lld:pubmed |
| pubmed-article:17088249 | pubmed:author | pubmed-author:HaegmanMiraM | lld:pubmed |
| pubmed-article:17088249 | pubmed:author | pubmed-author:VerstrepenLyn... | lld:pubmed |
| pubmed-article:17088249 | pubmed:author | pubmed-author:VerhelstKelly... | lld:pubmed |
| pubmed-article:17088249 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17088249 | pubmed:day | 5 | lld:pubmed |
| pubmed-article:17088249 | pubmed:volume | 282 | lld:pubmed |
| pubmed-article:17088249 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17088249 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17088249 | pubmed:pagination | 81-90 | lld:pubmed |
| pubmed-article:17088249 | pubmed:dateRevised | 2010-9-10 | lld:pubmed |
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| pubmed-article:17088249 | pubmed:meshHeading | pubmed-meshheading:17088249... | lld:pubmed |
| pubmed-article:17088249 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:17088249 | pubmed:articleTitle | LIND/ABIN-3 is a novel lipopolysaccharide-inducible inhibitor of NF-kappaB activation. | lld:pubmed |
| pubmed-article:17088249 | pubmed:affiliation | Unit of Molecular Signal Transduction in Inflammation, Department for Molecular Biomedical Research, Flanders Interuniversity Institute for Biotechnology, Ghent University, Belgium. | lld:pubmed |
| pubmed-article:17088249 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:17088249 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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