pubmed-article:18504435 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:18504435 | lifeskim:mentions | umls-concept:C0664336 | lld:lifeskim |
pubmed-article:18504435 | lifeskim:mentions | umls-concept:C1334468 | lld:lifeskim |
pubmed-article:18504435 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
pubmed-article:18504435 | lifeskim:mentions | umls-concept:C0178874 | lld:lifeskim |
pubmed-article:18504435 | lifeskim:mentions | umls-concept:C1414227 | lld:lifeskim |
pubmed-article:18504435 | lifeskim:mentions | umls-concept:C1704666 | lld:lifeskim |
pubmed-article:18504435 | lifeskim:mentions | umls-concept:C1517892 | lld:lifeskim |
pubmed-article:18504435 | lifeskim:mentions | umls-concept:C0208973 | lld:lifeskim |
pubmed-article:18504435 | pubmed:issue | 40 | lld:pubmed |
pubmed-article:18504435 | pubmed:dateCreated | 2008-9-11 | lld:pubmed |
pubmed-article:18504435 | pubmed:abstractText | Survivin is a prosurvival protein overexpressed in many cancers through mechanisms that remain poorly explored, and is implicated in control of tumor progression and resistance to cancer chemotherapeutics. Here, we report a critical role for survivin in the induction of apoptosis by transforming growth factor-beta (TGF-beta). We show that TGF-beta rapidly downregulates survivin expression in prostate epithelial cells, through a unique mechanism of transcriptional suppression involving Smads 2 and 3, Rb/E2F4, and the cell-cycle repressor elements CDE and CHR. This TGF-beta response is triggered through a Smad2/3-dependent hypophosphorylation of Rb and the subsequent association of the Rb/E2F4 repressive complex to CDE/CHR elements in the proximal region of the survivin promoter. Viral-mediated gene delivery experiments, involving overexpressing or silencing survivin, reveal critical roles of survivin in apoptosis induced by TGF-beta alone or in cooperation with cancer therapeutic agents. We propose a novel TGF-beta/Rb/survivin axis with a putative role in the functional switch of TGF-beta from tumor suppressor to tumor promoter. | lld:pubmed |
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pubmed-article:18504435 | pubmed:language | eng | lld:pubmed |
pubmed-article:18504435 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18504435 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:18504435 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:18504435 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:18504435 | pubmed:month | Sep | lld:pubmed |
pubmed-article:18504435 | pubmed:issn | 1476-5594 | lld:pubmed |
pubmed-article:18504435 | pubmed:author | pubmed-author:YangJJ | lld:pubmed |
pubmed-article:18504435 | pubmed:author | pubmed-author:SongKK | lld:pubmed |
pubmed-article:18504435 | pubmed:author | pubmed-author:JacksonM WMW | lld:pubmed |
pubmed-article:18504435 | pubmed:author | pubmed-author:KrebsT LTL | lld:pubmed |
pubmed-article:18504435 | pubmed:author | pubmed-author:DanielpourDD | lld:pubmed |
pubmed-article:18504435 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:18504435 | pubmed:day | 11 | lld:pubmed |
pubmed-article:18504435 | pubmed:volume | 27 | lld:pubmed |
pubmed-article:18504435 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:18504435 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:18504435 | pubmed:pagination | 5326-38 | lld:pubmed |
pubmed-article:18504435 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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