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This Article Accepted manuscript (PDF) All Versions of this Article: JME-08-0103v1 41/5/263    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Safe, S. Articles by Kim, K. PubMed PubMed Citation Articles by Safe, S. Articles by Kim, K.

S Safe, Veterinary Physiology & Pharmacology, Texas A&M University, College Station, 77843-4466, United States
K Kim, Institute of Biosciences and Technology, Texas A&M Health Science Center, Houston, United States

Correspondence: Stephen Safe, Email: ssafe{at}cvm.tamu.edu

Abstract

17β-Estradiol (E2) binds to the estrogen receptor (ER) to activate gene expression or repression and this involves both genomic (nuclear) and non-genomic (extranuclear pathways). Genomic pathways include the classical interactions of ligand-bound ER dimers with estrogen-responsive elements (EREs) in target gene promoters. ER-dependent activation of gene expression also involves DNA-bound ER which subsequently interacts with other DNA-bound transcriptions factors and direct ER-transcription factor (protein-protein) interactions where ER does not bind promoter DNA. Ligand-induced activation of ER/specificity protein (Sp) and ER/activating protein-1 [(AP-1) consisting of jun/fos] complexes are important pathways for modulating expression of a large number of genes. This review summarizes some of the characteristics of ER/Sp- and ER/AP-1-mediated transactivation which are dependent on ligand structure, cell context, ER-subtype (ER and ERβ), and Sp protein (Sp1, Sp3 and Sp4) and demonstrates that this non-classical genomic pathway is also functional in vivo.