pubmed-article:1315961 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:1315961 | lifeskim:mentions | umls-concept:C0021641 | lld:lifeskim |
pubmed-article:1315961 | lifeskim:mentions | umls-concept:C0017337 | lld:lifeskim |
pubmed-article:1315961 | lifeskim:mentions | umls-concept:C0001455 | lld:lifeskim |
pubmed-article:1315961 | lifeskim:mentions | umls-concept:C0017725 | lld:lifeskim |
pubmed-article:1315961 | lifeskim:mentions | umls-concept:C0086860 | lld:lifeskim |
pubmed-article:1315961 | lifeskim:mentions | umls-concept:C0034349 | lld:lifeskim |
pubmed-article:1315961 | pubmed:issue | 8 | lld:pubmed |
pubmed-article:1315961 | pubmed:dateCreated | 1992-6-5 | lld:pubmed |
pubmed-article:1315961 | pubmed:abstractText | The glucose/insulin response element of the L-pyruvate kinase gene is a perfect palindrome located from nt -168 to -144 with respect to the cap site. This element (L4) is partially homologous to MLTF binding sites. Its full efficiency requires cooperation with a contiguous binding site for HNF4, termed L3 and located from nt -145 to -125. In the presence of the L4 element contiguous to L3, cyclic AMP inhibits activity of the L-PK promoter while in its absence, or when the normal L4-L3 contiguity is modified, cyclic AMP behaves as a transcriptional activator that does not seem to be sequence-specific. Therefore, we propose that the mechanism of inhibition of the L-PK gene by cyclic AMP requires precise interactions between the nucleoprotein complex built up at sites L4 and L3 and other components of the L-PK transcription initiation complex. | lld:pubmed |
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pubmed-article:1315961 | pubmed:language | eng | lld:pubmed |
pubmed-article:1315961 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1315961 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:1315961 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:1315961 | pubmed:month | Apr | lld:pubmed |
pubmed-article:1315961 | pubmed:issn | 0305-1048 | lld:pubmed |
pubmed-article:1315961 | pubmed:author | pubmed-author:KahnAA | lld:pubmed |
pubmed-article:1315961 | pubmed:author | pubmed-author:RaymondjeanMM | lld:pubmed |
pubmed-article:1315961 | pubmed:author | pubmed-author:PuzenatNN | lld:pubmed |
pubmed-article:1315961 | pubmed:author | pubmed-author:BergotM OMO | lld:pubmed |
pubmed-article:1315961 | pubmed:author | pubmed-author:Diaz-GuerraM... | lld:pubmed |
pubmed-article:1315961 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:1315961 | pubmed:day | 25 | lld:pubmed |
pubmed-article:1315961 | pubmed:volume | 20 | lld:pubmed |
pubmed-article:1315961 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:1315961 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:1315961 | pubmed:pagination | 1871-7 | lld:pubmed |
pubmed-article:1315961 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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pubmed-article:1315961 | pubmed:year | 1992 | lld:pubmed |
pubmed-article:1315961 | pubmed:articleTitle | Cis-regulation of the L-type pyruvate kinase gene promoter by glucose, insulin and cyclic AMP. | lld:pubmed |
pubmed-article:1315961 | pubmed:affiliation | ICGM, Laboratoire de recherches en Génétique et pathologie Moléculaire, INSERM U.129, CHU Cochin, Paris, France. | lld:pubmed |
pubmed-article:1315961 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:1315961 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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