| pubmed-article:8662753 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8662753 | lifeskim:mentions | umls-concept:C0126732 | lld:lifeskim |
| pubmed-article:8662753 | lifeskim:mentions | umls-concept:C1367798 | lld:lifeskim |
| pubmed-article:8662753 | lifeskim:mentions | umls-concept:C1456820 | lld:lifeskim |
| pubmed-article:8662753 | lifeskim:mentions | umls-concept:C1367675 | lld:lifeskim |
| pubmed-article:8662753 | lifeskim:mentions | umls-concept:C0699900 | lld:lifeskim |
| pubmed-article:8662753 | lifeskim:mentions | umls-concept:C0243125 | lld:lifeskim |
| pubmed-article:8662753 | lifeskim:mentions | umls-concept:C1523116 | lld:lifeskim |
| pubmed-article:8662753 | lifeskim:mentions | umls-concept:C1314939 | lld:lifeskim |
| pubmed-article:8662753 | pubmed:issue | 22 | lld:pubmed |
| pubmed-article:8662753 | pubmed:dateCreated | 1996-8-15 | lld:pubmed |
| pubmed-article:8662753 | pubmed:abstractText | Signal-dependent activation of the transcription factor NF-kappaB is dominantly regulated by degradation of IkappaB-alpha protein. However, the signaling pathways that lead to the degradation are not clear. Here we report that mitogen-activated protein kinase/extracellular signal-regulated kinase kinase (MEK) kinase, an activator of stress-activated protein kinases/jun kinase-1 (SAPKs/JNK1), is involved in such signaling pathways. The transient overexpression of MEK kinase in NIH3T3 fibroblasts activates kappaB-CAT reporter expression in a synergistic manner with TNFalpha stimulation. In contrast, overexpression of kinase-negative MEK kinase suppresses TNFalpha-induced reporter expression. The overexpression of MEK kinase suppresses the inhibitory activity of co-transfected IkappaB-alpha on the kappaB-CAT or human immunodeficiency virus-long terminal repeat-luciferase reporter expression and causes the simultaneous disappearance of the overexpressed IkappaB-alpha. The disappearance of exogenous IkappaB-alpha by the overexpression of MEK kinase is prevented by calpain inhibitor-I, an inhibitor of IkappaB-alpha degradation. These results suggest that MEK kinase is a signal mediator involved in TNFalpha-induced NF-kappaB activation and that the activation of NF-kappaB by MEK kinase is regulated through the degradation of IkappaB-alpha. | lld:pubmed |
| pubmed-article:8662753 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8662753 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8662753 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:8662753 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8662753 | pubmed:month | May | lld:pubmed |
| pubmed-article:8662753 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:8662753 | pubmed:author | pubmed-author:OhnoSS | lld:pubmed |
| pubmed-article:8662753 | pubmed:author | pubmed-author:HiranoMM | lld:pubmed |
| pubmed-article:8662753 | pubmed:author | pubmed-author:AokiTT | lld:pubmed |
| pubmed-article:8662753 | pubmed:author | pubmed-author:HiraiSS | lld:pubmed |
| pubmed-article:8662753 | pubmed:author | pubmed-author:HosakaMM | lld:pubmed |
| pubmed-article:8662753 | pubmed:author | pubmed-author:InoueJJ | lld:pubmed |
| pubmed-article:8662753 | pubmed:author | pubmed-author:OsadaSS | lld:pubmed |
| pubmed-article:8662753 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8662753 | pubmed:day | 31 | lld:pubmed |
| pubmed-article:8662753 | pubmed:volume | 271 | lld:pubmed |
| pubmed-article:8662753 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8662753 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8662753 | pubmed:pagination | 13234-8 | lld:pubmed |
| pubmed-article:8662753 | pubmed:dateRevised | 2011-11-2 | lld:pubmed |
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| pubmed-article:8662753 | pubmed:meshHeading | pubmed-meshheading:8662753-... | lld:pubmed |
| pubmed-article:8662753 | pubmed:year | 1996 | lld:pubmed |
| pubmed-article:8662753 | pubmed:articleTitle | MEK kinase is involved in tumor necrosis factor alpha-induced NF-kappaB activation and degradation of IkappaB-alpha. | lld:pubmed |
| pubmed-article:8662753 | pubmed:affiliation | Department of Molecular Biology, Yokohama City University School of Medicine, 3-9 Fuku-ura, Kanazawa-ku, Yokohama 236, Japan. | lld:pubmed |
| pubmed-article:8662753 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8662753 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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