pubmed-article:11672436 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:11672436 | lifeskim:mentions | umls-concept:C0123256 | lld:lifeskim |
pubmed-article:11672436 | lifeskim:mentions | umls-concept:C0021641 | lld:lifeskim |
pubmed-article:11672436 | lifeskim:mentions | umls-concept:C0017755 | lld:lifeskim |
pubmed-article:11672436 | lifeskim:mentions | umls-concept:C1280500 | lld:lifeskim |
pubmed-article:11672436 | lifeskim:mentions | umls-concept:C0018270 | lld:lifeskim |
pubmed-article:11672436 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
pubmed-article:11672436 | lifeskim:mentions | umls-concept:C0031586 | lld:lifeskim |
pubmed-article:11672436 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
pubmed-article:11672436 | pubmed:issue | Pt 3 | lld:pubmed |
pubmed-article:11672436 | pubmed:dateCreated | 2001-10-23 | lld:pubmed |
pubmed-article:11672436 | pubmed:abstractText | Glucose-6-phosphatase (G6Pase) and insulin-like growth factor-binding protein-1 (IGFBP-1) genes contain a homologous promoter sequence that is required for gene repression by insulin. Interestingly, this element interacts with members of the forkhead family of transcription factors [e.g. HNF3 (hepatic nuclear factor 3), FKHR (forkhead in rhabdomyosarcoma)] in vitro, while insulin promotes the phosphorylation and inactivation of FKHR in a phosphatidylinositol 3-kinase- and protein kinase B (PKB)-dependent manner. This mechanism has been proposed to underlie insulin action on G6Pase and IGFBP-1 gene transcription. However, we find that treatment of cells with phorbol esters mimics the effect of insulin on G6Pase, but not IGFBP-1, gene expression. Indeed, phorbol ester treatment actually blocks the ability of insulin to repress IGFBP-1 gene expression. In addition, the action of phorbol esters is significantly reduced by inhibition of the p42/p44 mitogen-activated protein (MAP) kinase pathway. However insulin-induced phosphorylation of PKB or FKHR is not affected by the presence of phorbol esters. Therefore we suggest that activation of p42/p44 MAP kinases will reduce the sensitivity of the IGFBP-1 gene promoter, but not the G6Pase gene promoter, to insulin. Importantly, the activation of PKB and phosphorylation of FKHR is not, in itself, sufficient to reduce IGFBP-1 gene expression in the presence of phorbol esters. | lld:pubmed |
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pubmed-article:11672436 | pubmed:language | eng | lld:pubmed |
pubmed-article:11672436 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11672436 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:11672436 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:11672436 | pubmed:month | Nov | lld:pubmed |
pubmed-article:11672436 | pubmed:issn | 0264-6021 | lld:pubmed |
pubmed-article:11672436 | pubmed:author | pubmed-author:PatelSS | lld:pubmed |
pubmed-article:11672436 | pubmed:author | pubmed-author:Rei?PP | lld:pubmed |
pubmed-article:11672436 | pubmed:author | pubmed-author:SutherlandCC | lld:pubmed |
pubmed-article:11672436 | pubmed:author | pubmed-author:LochheadP APA | lld:pubmed |
pubmed-article:11672436 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:11672436 | pubmed:day | 1 | lld:pubmed |
pubmed-article:11672436 | pubmed:volume | 359 | lld:pubmed |
pubmed-article:11672436 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:11672436 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:11672436 | pubmed:pagination | 611-9 | lld:pubmed |
pubmed-article:11672436 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
pubmed-article:11672436 | pubmed:meshHeading | pubmed-meshheading:11672436... | lld:pubmed |
pubmed-article:11672436 | pubmed:meshHeading | pubmed-meshheading:11672436... | lld:pubmed |
pubmed-article:11672436 | pubmed:meshHeading | pubmed-meshheading:11672436... | lld:pubmed |