| pubmed-article:15277532 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15277532 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
| pubmed-article:15277532 | lifeskim:mentions | umls-concept:C1367731 | lld:lifeskim |
| pubmed-article:15277532 | lifeskim:mentions | umls-concept:C1150587 | lld:lifeskim |
| pubmed-article:15277532 | lifeskim:mentions | umls-concept:C1705632 | lld:lifeskim |
| pubmed-article:15277532 | lifeskim:mentions | umls-concept:C1417830 | lld:lifeskim |
| pubmed-article:15277532 | lifeskim:mentions | umls-concept:C0086597 | lld:lifeskim |
| pubmed-article:15277532 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:15277532 | pubmed:issue | 37 | lld:pubmed |
| pubmed-article:15277532 | pubmed:dateCreated | 2004-9-6 | lld:pubmed |
| pubmed-article:15277532 | pubmed:abstractText | Sef was recently identified as a negative regulator of fibroblast growth factor (FGF) signaling in a genetic screen of zebrafish and subsequently in mouse and humans. By inhibiting FGFR1 tyrosine phosphorylation and/or Ras downstream events, Sef inhibits FGF-mediated ERK activation and cell proliferation as well as PC12 cell differentiation. Here we show that Sef and a deletion mutant of Sef lacking the extracellular domain (SefIC) physically interact with TAK1 (transforming growth factor-beta-associated kinase) and activate JNK through a TAK1-MKK4-JNK pathway. Sef and SefIC overexpression also resulted in apoptotic cell death, while dominant negative forms of MKK4 and TAK1 blocked Sef-mediated JNK activation and attendant 293T cell apoptosis. These investigations reveal a novel activating function of Sef that is distinct from its inhibitory effect on FGF receptor signaling and ERK activation. | lld:pubmed |
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| pubmed-article:15277532 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:15277532 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:15277532 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15277532 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:15277532 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:15277532 | pubmed:author | pubmed-author:MitchellJaneJ | lld:pubmed |
| pubmed-article:15277532 | pubmed:author | pubmed-author:FrieselRobert... | lld:pubmed |
| pubmed-article:15277532 | pubmed:author | pubmed-author:KovalenkoDmit... | lld:pubmed |
| pubmed-article:15277532 | pubmed:author | pubmed-author:YangXuehuiX | lld:pubmed |
| pubmed-article:15277532 | pubmed:author | pubmed-author:NadeauRobert... | lld:pubmed |
| pubmed-article:15277532 | pubmed:author | pubmed-author:HarkinsLauren... | lld:pubmed |
| pubmed-article:15277532 | pubmed:author | pubmed-author:ChenPei-YuPY | lld:pubmed |
| pubmed-article:15277532 | pubmed:author | pubmed-author:ZubanovaOlgaO | lld:pubmed |
| pubmed-article:15277532 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15277532 | pubmed:day | 10 | lld:pubmed |
| pubmed-article:15277532 | pubmed:volume | 279 | lld:pubmed |
| pubmed-article:15277532 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15277532 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15277532 | pubmed:pagination | 38099-102 | lld:pubmed |
| pubmed-article:15277532 | pubmed:dateRevised | 2011-11-2 | lld:pubmed |
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| pubmed-article:15277532 | pubmed:year | 2004 | lld:pubmed |
| pubmed-article:15277532 | pubmed:articleTitle | Sef interacts with TAK1 and mediates JNK activation and apoptosis. | lld:pubmed |
| pubmed-article:15277532 | pubmed:affiliation | Center for Molecular Medicine, Maine Medical Center Research Institute, Scarborough, Maine 04074, USA. | lld:pubmed |
| pubmed-article:15277532 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15277532 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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