| pubmed-article:10748240 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10748240 | lifeskim:mentions | umls-concept:C0384648 | lld:lifeskim |
| pubmed-article:10748240 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
| pubmed-article:10748240 | lifeskim:mentions | umls-concept:C1514873 | lld:lifeskim |
| pubmed-article:10748240 | lifeskim:mentions | umls-concept:C1449799 | lld:lifeskim |
| pubmed-article:10748240 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:10748240 | pubmed:dateCreated | 2000-6-8 | lld:pubmed |
| pubmed-article:10748240 | pubmed:abstractText | Signaling through its widely distributed cell surface receptor, interleukin (IL)-17 enhances the transcription of genes encoding proinflammatory molecules. Although it has been well documented that IL-17 activates the transcription factor nuclear factor (NF)-kappaB and c-Jun NH(2)-terminal kinase (JNK), the upstream signaling events are largely unknown. Here we report the requirement of tumor necrosis factor receptor-associated factor (TRAF)6 in IL-17-induced NF-kappaB and JNK activation. In embryonic fibroblasts (EFs) derived from TRAF6 knockout mice, IL-17 failed to activate the IkappaB kinases (IKKs) and JNK. Consequently, IL-17-induced IL-6 and intercellular adhesion molecule 1 expression in the TRAF6-deficient cells was abolished. Lack of TRAF6 appeared to be the sole defect responsible for the observed failure to respond to IL-17, because transient transfection of TRAF6 expression plasmid into the TRAF6-deficient cells restored IL-17-induced NF-kappaB activation in a luciferase reporter assay. Furthermore, the levels of IL-17 receptor (IL-17R) on the TRAF6-deficient EFs were comparable to those on the wild-type control cells. Defect in IL-17 response was not observed in TRAF2-deficient EFs. Moreover, when TRAF6 and IL-17R were coexpressed in 293 cells, TRAF6 coimmunoprecipitated with IL-17R. Together, these results indicate that TRAF6, but not TRAF2, is a crucial component in the IL-17 signaling pathway leading to proinflammatory responses. | lld:pubmed |
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| pubmed-article:10748240 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10748240 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10748240 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:10748240 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:10748240 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10748240 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:10748240 | pubmed:issn | 0022-1007 | lld:pubmed |
| pubmed-article:10748240 | pubmed:author | pubmed-author:YamaguchiKK | lld:pubmed |
| pubmed-article:10748240 | pubmed:author | pubmed-author:SchwandnerRR | lld:pubmed |
| pubmed-article:10748240 | pubmed:author | pubmed-author:CaoZZ | lld:pubmed |
| pubmed-article:10748240 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10748240 | pubmed:day | 3 | lld:pubmed |
| pubmed-article:10748240 | pubmed:volume | 191 | lld:pubmed |
| pubmed-article:10748240 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10748240 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10748240 | pubmed:pagination | 1233-40 | lld:pubmed |
| pubmed-article:10748240 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
