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¹ Department of Cellular Biology,
² Faculty of Pharmacy and
³ Centro Sanitario, University of Calabria, Via Pietro Bucci, cubo 4c, 87030 Arcavacata di Rende (CS), Italy

(Requests for offprints should be addressed to S Ando’ at the Department of Cellular Biology, University of Calabria; Email: sebastiano.ando{at}unical.it)

^* (M L Panno and L Mauro contributed equally to this work)

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/ER and Sp1.

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