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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.

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