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This version published online on February 3, 2005
Molecular Endocrinology, doi:10.1210/me.2004-0486
A more recent version of this article appeared on April 1, 2005
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Submitted on December 7, 2004
Accepted on January 25, 2005

Mechanisms of Estrogen Receptor Signaling: Convergence of Genomic and Non-Genomic Actions on Target Genes

Linda Björnström and Maria Sjöberg*

Dept. of Cell and Molecular Biology, Karolinska Institutet, SE-171 77 Stockholm

Estrogen receptors (ERs) act by regulating transcriptional processes. The classical mechanism of ER action involves estrogen binding to receptors in the nucleus, after which the receptors dimerize and bind to specific response elements known as estrogen response elements (EREs) located in the promoters of target genes. However, ERs can also regulate gene expression without directly binding to DNA. This occurs through protein-protein interactions with other DNA-binding transcription factors in the nucleus. In addition, membrane-associated ERs mediate non-genomic actions of estrogens, which can lead both to altered functions of proteins in the cytoplasm and to regulation of gene expression. The latter two mechanisms of ER action enable a broader range of genes to be regulated than the range that can be regulated by the classical mechanism of ER action alone. This review surveys our knowledge about the molecular mechanism by which ERs regulate the expression of genes that do not contain EREs, and it gives examples of the ways in which the genomic and non-genomic actions of ERs on target genes converge. Genomic and non-genomic actions of ERs that do not depend on EREs influence the physiology of many target tissues, and thus, increasing our understanding of the molecular mechanisms behind these actions is highly relevant for the development of novel drugs that target specific receptor actions.

NURSA Molecule Pages Link:

Nuclear Receptors:   ERα  |  ERβ
Coregulators:   STAT3  |  CAV1  |  PELP1
Ligands:   17β-Estradiol



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