| pubmed-article:10921914 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10921914 | lifeskim:mentions | umls-concept:C0079904 | lld:lifeskim |
| pubmed-article:10921914 | lifeskim:mentions | umls-concept:C1704675 | lld:lifeskim |
| pubmed-article:10921914 | lifeskim:mentions | umls-concept:C0441655 | lld:lifeskim |
| pubmed-article:10921914 | lifeskim:mentions | umls-concept:C1417014 | lld:lifeskim |
| pubmed-article:10921914 | lifeskim:mentions | umls-concept:C0332453 | lld:lifeskim |
| pubmed-article:10921914 | pubmed:issue | 42 | lld:pubmed |
| pubmed-article:10921914 | pubmed:dateCreated | 2000-11-20 | lld:pubmed |
| pubmed-article:10921914 | pubmed:abstractText | Apoptosis signal-regulating kinase 1 (ASK1) is a member of the MAPKKK family in the JNK and p38 mitogen-activated protein kinase cascades and critically involved in stress- and cytokine-induced apoptosis. The transcription factor nuclear factor-kappaB (NF-kappaB) is a pivotal regulator of immune and inflammatory responses and exerts anti-apoptotic roles in various cells. Here we show that ASK1 directly interacts with transforming growth factor-beta-activated kinase 1 (TAK1), another MAPKKK that has been identified as a signaling intermediate in the interleukin 1 (IL-1)-induced NF-kappaB pathway as well as the transforming growth factor-beta superfamily-induced JNK/p38 pathway. Overexpression of ASK1 inhibits IL-1-, TRAF6-, or TAK1-induced, but not NF-kappaB-inducing kinase-induced, NF-kappaB activation. ASK1 dissociates TAK1 but not NF-kappaB-inducing kinase from TRAF6. Moreover, IL-1-induced complex formation of endogenous TAK1 and TRAF6 was blocked by ASK1 overexpression. It thus appears that the inhibition of NF-kappaB by ASK1 may result at least in part from the disruption of the TRAF6.TAK1 complex formation in the IL-1 signaling pathway. These results provide a new insight in the mode of action of MAPKKK family members; two distinct MAPKKKs in the same MAP kinase cascades directly interact and exert opposite effects in another signaling pathway, NF-kappaB. | lld:pubmed |
| pubmed-article:10921914 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10921914 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10921914 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:10921914 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10921914 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:10921914 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10921914 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:10921914 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:10921914 | pubmed:author | pubmed-author:TakedaKK | lld:pubmed |
| pubmed-article:10921914 | pubmed:author | pubmed-author:MatsumotoKK | lld:pubmed |
| pubmed-article:10921914 | pubmed:author | pubmed-author:SaitohMM | lld:pubmed |
| pubmed-article:10921914 | pubmed:author | pubmed-author:AmagasaTT | lld:pubmed |
| pubmed-article:10921914 | pubmed:author | pubmed-author:IchijoHH | lld:pubmed |
| pubmed-article:10921914 | pubmed:author | pubmed-author:MochidaYY | lld:pubmed |
| pubmed-article:10921914 | pubmed:author | pubmed-author:Ninomiya-Tsuj... | lld:pubmed |
| pubmed-article:10921914 | pubmed:author | pubmed-author:NishitohHH | lld:pubmed |
| pubmed-article:10921914 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10921914 | pubmed:day | 20 | lld:pubmed |
| pubmed-article:10921914 | pubmed:volume | 275 | lld:pubmed |
| pubmed-article:10921914 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10921914 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10921914 | pubmed:pagination | 32747-52 | lld:pubmed |
| pubmed-article:10921914 | pubmed:dateRevised | 2011-11-2 | lld:pubmed |
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| pubmed-article:10921914 | pubmed:year | 2000 | lld:pubmed |
| pubmed-article:10921914 | pubmed:articleTitle | ASK1 inhibits interleukin-1-induced NF-kappa B activity through disruption of TRAF6-TAK1 interaction. | lld:pubmed |
| pubmed-article:10921914 | pubmed:affiliation | Laboratory of Cell Signaling, Department of Hard Tissue Engineering, Division of Bio-Matrix, Tokyo, Japan. | lld:pubmed |
| pubmed-article:10921914 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10921914 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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