| pubmed-article:15572679 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15572679 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:15572679 | lifeskim:mentions | umls-concept:C0597357 | lld:lifeskim |
| pubmed-article:15572679 | lifeskim:mentions | umls-concept:C1456820 | lld:lifeskim |
| pubmed-article:15572679 | lifeskim:mentions | umls-concept:C1442513 | lld:lifeskim |
| pubmed-article:15572679 | lifeskim:mentions | umls-concept:C1150582 | lld:lifeskim |
| pubmed-article:15572679 | lifeskim:mentions | umls-concept:C1523116 | lld:lifeskim |
| pubmed-article:15572679 | pubmed:issue | 24 | lld:pubmed |
| pubmed-article:15572679 | pubmed:dateCreated | 2004-12-1 | lld:pubmed |
| pubmed-article:15572679 | pubmed:abstractText | Receptor-interacting protein (RIP) plays a critical role in tumor necrosis factor alpha (TNF-alpha)-induced NF-kappaB activation. However, the mechanism by which RIP mediates TNF-alpha-induced signal transduction is not fully understood. In this study, we reconstituted RIP-deficient Jurkat T cells with a fusion protein composed of full-length MEKK3 and the death domain of RIP (MEKK3-DD). In these cells, MEKK3-DD substitutes for RIP and directly associates with TRADD in TNF receptor complexes following TNF-alpha stimulation. We found that TNF-alpha-induced NF-kappaB activation was fully restored by MEKK3-DD in these cells. In contrast, expression of a fusion protein composed of NEMO, a component of the IkappaB kinase complex, and the death domain of RIP (NEMO-DD) cannot restore TNF-alpha-induced NF-kappaB activation in RIP-deficient cells. These results indicate that the role of RIP is to specifically recruit MEKK3 to the TNF-alpha receptor complex, whereas the forced recruitment of NEMO to the TNF-alpha receptor complex is insufficient for TNF-alpha-induced NF-kappaB activation. Although MEKK2 has a high degree of homology with MEKK3, MEKK2-DD, unlike MEKK3-DD, also fails to restore TNF-alpha-induced NF-kappaB activation in RIP-deficient cells, indicating that RIP-dependent recruitment of MEKK3 plays a specific role in TNF-alpha signaling. | lld:pubmed |
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| pubmed-article:15572679 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15572679 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15572679 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:15572679 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15572679 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:15572679 | pubmed:issn | 0270-7306 | lld:pubmed |
| pubmed-article:15572679 | pubmed:author | pubmed-author:KekL PLP | lld:pubmed |
| pubmed-article:15572679 | pubmed:author | pubmed-author:LinXinX | lld:pubmed |
| pubmed-article:15572679 | pubmed:author | pubmed-author:GeleziunasRom... | lld:pubmed |
| pubmed-article:15572679 | pubmed:author | pubmed-author:BlonskaMarzen... | lld:pubmed |
| pubmed-article:15572679 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15572679 | pubmed:volume | 24 | lld:pubmed |
| pubmed-article:15572679 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15572679 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15572679 | pubmed:pagination | 10757-65 | lld:pubmed |
| pubmed-article:15572679 | pubmed:dateRevised | 2011-11-2 | lld:pubmed |
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| pubmed-article:15572679 | pubmed:year | 2004 | lld:pubmed |
| pubmed-article:15572679 | pubmed:articleTitle | Restoration of NF-kappaB activation by tumor necrosis factor alpha receptor complex-targeted MEKK3 in receptor-interacting protein-deficient cells. | lld:pubmed |
| pubmed-article:15572679 | pubmed:affiliation | Department of Microbiology and Immunology, School of Medicine and Biomedical Sciences, University at Buffalo, SUNY, 138 Farber Hall, 3435 Main St., Buffalo, NY 14214, USA. | lld:pubmed |
| pubmed-article:15572679 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15572679 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:15572679 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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