| pubmed-article:16461930 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16461930 | lifeskim:mentions | umls-concept:C0025914 | lld:lifeskim |
| pubmed-article:16461930 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:16461930 | lifeskim:mentions | umls-concept:C1335858 | lld:lifeskim |
| pubmed-article:16461930 | lifeskim:mentions | umls-concept:C0665341 | lld:lifeskim |
| pubmed-article:16461930 | lifeskim:mentions | umls-concept:C1704675 | lld:lifeskim |
| pubmed-article:16461930 | lifeskim:mentions | umls-concept:C0123658 | lld:lifeskim |
| pubmed-article:16461930 | lifeskim:mentions | umls-concept:C0086860 | lld:lifeskim |
| pubmed-article:16461930 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:16461930 | lifeskim:mentions | umls-concept:C1517488 | lld:lifeskim |
| pubmed-article:16461930 | lifeskim:mentions | umls-concept:C0332120 | lld:lifeskim |
| pubmed-article:16461930 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:16461930 | pubmed:dateCreated | 2006-2-7 | lld:pubmed |
| pubmed-article:16461930 | pubmed:abstractText | In the present study, the molecular mechanism underlying the up-regulatory effect of estradiol (E2) on mouse insulin receptor substrate-1 (IRS-1) promoter was investigated in CHO cells on which the same promoter had first been functionally characterized. The mouse IRS-1 promoter bears four consensus half Estrogen Responsive Elements (ERE) sequences and thirteen AP-1- and ten Sp1-binding elements. We performed molecular dissection of this promoter gene providing 3' different deleted constructs, containing the same AP-1 rich region with a progressively increased number of ERE half sites located downstream. None of these constructs was responsive to E2, while a downstream region (nt -1420 to -160) rich in GC elements was induced by E2. However, the latter region lost its intrinsic E2 responsiveness when the whole IRS-1 promoter was mutated for deletion in all four ERE half sites. Deletion analysis of the ERE half sites demonstrated that only ERE located at the position -1500 to -1495, close to the GC-rich region, was able to maintain the induced activatory effect of E2 on the IRS-1 gene. Electrophoretic mobility shift and chromatin immunoprecipitation assays identified the region containing the half ERE/Sp1 (nt -1500 to -1477) as the one conferring E2 responsiveness to the whole promoter. This effect occurs through the functional interaction between E2/ERalpha and Sp1. | lld:pubmed |
| pubmed-article:16461930 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16461930 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16461930 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:16461930 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16461930 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16461930 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16461930 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16461930 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16461930 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16461930 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16461930 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16461930 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:16461930 | pubmed:issn | 0952-5041 | lld:pubmed |
| pubmed-article:16461930 | pubmed:author | pubmed-author:GiordanoFF | lld:pubmed |
| pubmed-article:16461930 | pubmed:author | pubmed-author:MauriJJ | lld:pubmed |
| pubmed-article:16461930 | pubmed:author | pubmed-author:AndòSS | lld:pubmed |
| pubmed-article:16461930 | pubmed:author | pubmed-author:MorelliCC | lld:pubmed |
| pubmed-article:16461930 | pubmed:author | pubmed-author:MarsicoSS | lld:pubmed |
| pubmed-article:16461930 | pubmed:author | pubmed-author:RizzuDD | lld:pubmed |
| pubmed-article:16461930 | pubmed:author | pubmed-author:SalernoMM | lld:pubmed |
| pubmed-article:16461930 | pubmed:author | pubmed-author:PannoM LML | lld:pubmed |
| pubmed-article:16461930 | pubmed:author | pubmed-author:BellizziDD | lld:pubmed |
| pubmed-article:16461930 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16461930 | pubmed:volume | 36 | lld:pubmed |
| pubmed-article:16461930 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16461930 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16461930 | pubmed:pagination | 91-105 | lld:pubmed |
| pubmed-article:16461930 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:16461930 | pubmed:meshHeading | pubmed-meshheading:16461930... | lld:pubmed |
| pubmed-article:16461930 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:16461930 | pubmed:articleTitle | Evidence that the mouse insulin receptor substrate-1 belongs to the gene family on which the promoter is activated by estrogen receptor alpha through its interaction with Sp1. | lld:pubmed |
| pubmed-article:16461930 | pubmed:affiliation | Department of Cellular Biology, University of Calabria, Italy. | lld:pubmed |
| pubmed-article:16461930 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16461930 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
