| pubmed-article:16636667 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16636667 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:16636667 | lifeskim:mentions | umls-concept:C0376358 | lld:lifeskim |
| pubmed-article:16636667 | lifeskim:mentions | umls-concept:C0919453 | lld:lifeskim |
| pubmed-article:16636667 | lifeskim:mentions | umls-concept:C0033572 | lld:lifeskim |
| pubmed-article:16636667 | lifeskim:mentions | umls-concept:C0033684 | lld:lifeskim |
| pubmed-article:16636667 | lifeskim:mentions | umls-concept:C0040690 | lld:lifeskim |
| pubmed-article:16636667 | lifeskim:mentions | umls-concept:C0018270 | lld:lifeskim |
| pubmed-article:16636667 | lifeskim:mentions | umls-concept:C1422480 | lld:lifeskim |
| pubmed-article:16636667 | lifeskim:mentions | umls-concept:C0237477 | lld:lifeskim |
| pubmed-article:16636667 | lifeskim:mentions | umls-concept:C1704222 | lld:lifeskim |
| pubmed-article:16636667 | pubmed:issue | 41 | lld:pubmed |
| pubmed-article:16636667 | pubmed:dateCreated | 2006-9-14 | lld:pubmed |
| pubmed-article:16636667 | pubmed:abstractText | Transforming growth factor-beta (TGF-beta) elicits a potent growth inhibitory effect on many normal cells by binding to specific serine/threonine kinase receptors and activating specific Smad proteins, which regulate the expression of cell cycle genes, including the p21 cyclin-dependent kinase (CDK) inhibitor gene. Interestingly, cancer cells are often insensitive to the anti-mitogenic effects of TGF-beta for which the molecular mechanisms are not well understood. In this study, we found that the candidate prostate cancer susceptibility gene ELAC2 potentiates TGF-beta/Smad-induced transcriptional responses. ELAC2 associates with activated Smad2; the C-terminal MH2 domain of Smad2 interacts with the N-terminal region of ELAC2. Small interfering siRNA-mediated knock-down of ELAC2 in prostate cells suppressed TGF-beta-induced growth arrest. Moreover, ELAC2 was shown to specifically associate with the nuclear Smad2 partner, FAST-1 and to potentiate the interaction of activated Smad2 with transcription factor Sp1. Furthermore, activation of the p21 CDK inhibitor promoter by TGF-beta is potentiated by ELAC2. Taken together our data indicate an important transcriptional scaffold function for ELAC2 in TGF-beta/Smad signaling mediated growth arrest. | lld:pubmed |
| pubmed-article:16636667 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16636667 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16636667 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:16636667 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16636667 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16636667 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:16636667 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16636667 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16636667 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:16636667 | pubmed:issn | 0950-9232 | lld:pubmed |
| pubmed-article:16636667 | pubmed:author | pubmed-author:WatanabeYY | lld:pubmed |
| pubmed-article:16636667 | pubmed:author | pubmed-author:KatoMM | lld:pubmed |
| pubmed-article:16636667 | pubmed:author | pubmed-author:ItohSS | lld:pubmed |
| pubmed-article:16636667 | pubmed:author | pubmed-author:KoikeSS | lld:pubmed |
| pubmed-article:16636667 | pubmed:author | pubmed-author:LoweJ AJA | lld:pubmed |
| pubmed-article:16636667 | pubmed:author | pubmed-author:ItouSS | lld:pubmed |
| pubmed-article:16636667 | pubmed:author | pubmed-author:DanielpourDD | lld:pubmed |
| pubmed-article:16636667 | pubmed:author | pubmed-author:ten DijkePP | lld:pubmed |
| pubmed-article:16636667 | pubmed:author | pubmed-author:InamitsuMM | lld:pubmed |
| pubmed-article:16636667 | pubmed:author | pubmed-author:DennlerSS | lld:pubmed |
| pubmed-article:16636667 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16636667 | pubmed:day | 14 | lld:pubmed |
| pubmed-article:16636667 | pubmed:volume | 25 | lld:pubmed |
| pubmed-article:16636667 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16636667 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16636667 | pubmed:pagination | 5591-600 | lld:pubmed |
| pubmed-article:16636667 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:16636667 | pubmed:meshHeading | pubmed-meshheading:16636667... | lld:pubmed |
| pubmed-article:16636667 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:16636667 | pubmed:articleTitle | ELAC2, a putative prostate cancer susceptibility gene product, potentiates TGF-beta/Smad-induced growth arrest of prostate cells. | lld:pubmed |
| pubmed-article:16636667 | pubmed:affiliation | Department of Experimental Pathology, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Ibaraki, Japan. | lld:pubmed |
| pubmed-article:16636667 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16636667 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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