| pubmed-article:14517280 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:14517280 | lifeskim:mentions | umls-concept:C1378703 | lld:lifeskim |
| pubmed-article:14517280 | lifeskim:mentions | umls-concept:C1518174 | lld:lifeskim |
| pubmed-article:14517280 | lifeskim:mentions | umls-concept:C0085177 | lld:lifeskim |
| pubmed-article:14517280 | lifeskim:mentions | umls-concept:C0079419 | lld:lifeskim |
| pubmed-article:14517280 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:14517280 | lifeskim:mentions | umls-concept:C1414371 | lld:lifeskim |
| pubmed-article:14517280 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
| pubmed-article:14517280 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
| pubmed-article:14517280 | pubmed:issue | 20 | lld:pubmed |
| pubmed-article:14517280 | pubmed:dateCreated | 2003-9-30 | lld:pubmed |
| pubmed-article:14517280 | pubmed:abstractText | A recent analysis of gene expression in renal cell carcinoma cells led to the identification of mRNAs whose translation was dependent on the presence of the von Hippel-Lindau (VHL) tumor suppressor gene product, pVHL. Here, we investigate the finding that pVHL-expressing RCC cells (VHL(+)) exhibited elevated levels of polysome-associated p53 mRNA and increased p53 protein levels compared with VHL-defective (VHL(-)) cells. Our findings indicate that p53 translation is specifically heightened in VHL(+) cells, given that (i) p53 mRNA abundance in VHL(+) and VHL(-) cells was comparable, (ii) p53 degradation did not significantly influence p53 expression, and (iii) p53 synthesis was markedly induced in VHL(+) cells. Electrophoretic mobility shift and immunoprecipitation assays to detect endogenous and radiolabeled p53 transcripts revealed that the RNA-binding protein HuR, previously shown to regulate mRNA turnover and translation, was capable of binding to the 3' untranslated region of the p53 mRNA in a VHL-dependent fashion. Interestingly, while whole-cell levels of HuR in VHL(+) and VHL(-) cells were comparable, HuR was markedly more abundant in the cytoplasmic and polysome-associated fractions of VHL(+) cells. In keeping with earlier reports, the elevated cytoplasmic HuR in VHL(+) cells was likely due to the reduced AMP-activated kinase activity in these cells. Demonstration that HuR indeed contributed to the increased expression of p53 in VHL(+) cells was obtained through use of RNA interference, which effectively reduced HuR expression and in turn caused marked decreases in p53 translation and p53 abundance. Taken together, our findings support a role for pVHL in elevating p53 expression, implicate HuR in enhancing VHL-mediated p53 translation, and suggest that VHL-mediated p53 upregulation may contribute to pVHL's tumor suppressive functions in renal cell carcinoma. | lld:pubmed |
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| pubmed-article:14517280 | pubmed:language | eng | lld:pubmed |
| pubmed-article:14517280 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14517280 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:14517280 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:14517280 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:14517280 | pubmed:issn | 0270-7306 | lld:pubmed |
| pubmed-article:14517280 | pubmed:author | pubmed-author:GorospeMyriam... | lld:pubmed |
| pubmed-article:14517280 | pubmed:author | pubmed-author:DeckerJochenJ | lld:pubmed |
| pubmed-article:14517280 | pubmed:author | pubmed-author:WangWengongW | lld:pubmed |
| pubmed-article:14517280 | pubmed:author | pubmed-author:FanJinshuiJ | lld:pubmed |
| pubmed-article:14517280 | pubmed:author | pubmed-author:MartindaleJen... | lld:pubmed |
| pubmed-article:14517280 | pubmed:author | pubmed-author:GalbánStefani... | lld:pubmed |
| pubmed-article:14517280 | pubmed:author | pubmed-author:López de... | lld:pubmed |
| pubmed-article:14517280 | pubmed:author | pubmed-author:Mazan-Mamczar... | lld:pubmed |
