| pubmed-article:14710354 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:14710354 | lifeskim:mentions | umls-concept:C0007600 | lld:lifeskim |
| pubmed-article:14710354 | lifeskim:mentions | umls-concept:C0376358 | lld:lifeskim |
| pubmed-article:14710354 | lifeskim:mentions | umls-concept:C0334227 | lld:lifeskim |
| pubmed-article:14710354 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
| pubmed-article:14710354 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
| pubmed-article:14710354 | lifeskim:mentions | umls-concept:C1549809 | lld:lifeskim |
| pubmed-article:14710354 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:14710354 | pubmed:issue | 11-12 | lld:pubmed |
| pubmed-article:14710354 | pubmed:dateCreated | 2004-1-7 | lld:pubmed |
| pubmed-article:14710354 | pubmed:abstractText | The type I insulin-like growth factor receptor (IGF-IR) plays a critical role in signaling survival and proliferation in many cell types. Activation of IGF-IR by its ligands promotes cell proliferation via mitogen-activated protein kinase (MAPK) cascade and cell survival via phosphoinositide 3-kinase (PI3K) cascade. The IGF-IR emerges as a powerful growth factor for many tumor cells. A truncated IGF-IR 486/STOP, described as a dominant negative IGF-IR mutant, was shown to induce apoptosis and inhibit tumor growth in vivo while endogenous IGF-IR was activated. To investigate the mechanism(s) of the action of 486/STOP, we have introduced 486/STOP into the prostate tumor model cell line M12 and its derivative M12lisn that expresses high levels of wild type IGF-IR. We have found that 486/STOP induces apoptosis in M12 and M12lisn cells in culture and that 486/STOP acts through activation of the pro-apoptotic p38-MAPK without interfering with wild type IGF-IR activation. In addition, our results have indicated that 486/STOP induced activation of p38-MAPK increases through activation of endogenous IGF-IR. These data suggest that activation of the IGF-IR by 486/STOP can selectively enhance the previously reported IGF-IR pro-apoptotic signaling pathways. | lld:pubmed |
| pubmed-article:14710354 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14710354 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14710354 | pubmed:language | eng | lld:pubmed |
| pubmed-article:14710354 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14710354 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:14710354 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14710354 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14710354 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14710354 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:14710354 | pubmed:issn | 0018-5043 | lld:pubmed |
| pubmed-article:14710354 | pubmed:author | pubmed-author:PlymateS RSR | lld:pubmed |
| pubmed-article:14710354 | pubmed:author | pubmed-author:WuJJ | lld:pubmed |
| pubmed-article:14710354 | pubmed:author | pubmed-author:HaugkKK | lld:pubmed |
| pubmed-article:14710354 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:14710354 | pubmed:volume | 35 | lld:pubmed |
| pubmed-article:14710354 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:14710354 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:14710354 | pubmed:pagination | 751-7 | lld:pubmed |
| pubmed-article:14710354 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
| pubmed-article:14710354 | pubmed:meshHeading | pubmed-meshheading:14710354... | lld:pubmed |
| pubmed-article:14710354 | pubmed:meshHeading | pubmed-meshheading:14710354... | lld:pubmed |
| pubmed-article:14710354 | pubmed:meshHeading | pubmed-meshheading:14710354... | lld:pubmed |
| pubmed-article:14710354 | pubmed:meshHeading | pubmed-meshheading:14710354... | lld:pubmed |
| pubmed-article:14710354 | pubmed:meshHeading | pubmed-meshheading:14710354... | lld:pubmed |
| pubmed-article:14710354 | pubmed:meshHeading | pubmed-meshheading:14710354... | lld:pubmed |
| pubmed-article:14710354 | pubmed:meshHeading | pubmed-meshheading:14710354... | lld:pubmed |
| pubmed-article:14710354 | pubmed:meshHeading | pubmed-meshheading:14710354... | lld:pubmed |
| pubmed-article:14710354 | pubmed:meshHeading | pubmed-meshheading:14710354... | lld:pubmed |
| pubmed-article:14710354 | pubmed:meshHeading | pubmed-meshheading:14710354... | lld:pubmed |
| pubmed-article:14710354 | pubmed:meshHeading | pubmed-meshheading:14710354... | lld:pubmed |
| pubmed-article:14710354 | pubmed:meshHeading | pubmed-meshheading:14710354... | lld:pubmed |
| pubmed-article:14710354 | pubmed:articleTitle | Activation of pro-apoptotic p38-MAPK pathway in the prostate cancer cell line M12 expressing a truncated IGF-IR. | lld:pubmed |
| pubmed-article:14710354 | pubmed:affiliation | Department of Medicine, Division of Gerontology and Geriatric Medicine, University of Washington, Seattle, WA 98104, USA. | lld:pubmed |
| pubmed-article:14710354 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:14710354 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:14710354 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
| entrez-gene:3480 | entrezgene:pubmed | pubmed-article:14710354 | lld:entrezgene |
| http://linkedlifedata.com/r... | entrezgene:pubmed | pubmed-article:14710354 | lld:entrezgene |
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| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:14710354 | lld:pubmed |
