Linked Life Data

16461930

Source:http://linkedlifedata.com/resource/pubmed/id/16461930

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2006-2-7
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0952-5041
pubmed:author
pubmed:issnType
Print
pubmed:volume
36
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
91-105
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:16461930-Animals, pubmed-meshheading:16461930-Base Sequence, pubmed-meshheading:16461930-Blotting, Western, pubmed-meshheading:16461930-CHO Cells, pubmed-meshheading:16461930-Cell Line, Tumor, pubmed-meshheading:16461930-Cricetinae, pubmed-meshheading:16461930-DNA Primers, pubmed-meshheading:16461930-Electrophoretic Mobility Shift Assay, pubmed-meshheading:16461930-Estrogen Receptor alpha, pubmed-meshheading:16461930-Humans, pubmed-meshheading:16461930-Insulin Receptor Substrate Proteins, pubmed-meshheading:16461930-Mice, pubmed-meshheading:16461930-Mutagenesis, Site-Directed, pubmed-meshheading:16461930-Phosphoproteins, pubmed-meshheading:16461930-Promoter Regions, Genetic, pubmed-meshheading:16461930-Protein Binding, pubmed-meshheading:16461930-Sp1 Transcription Factor
pubmed:year
2006
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.
pubmed:affiliation
Department of Cellular Biology, University of Calabria, Italy.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't