Mechanisms of estrogen signaling and gene expression via GPR30

Mol Cell Endocrinol. 2009 Sep 24;308(1-2):32-8. doi: 10.1016/j.mce.2009.03.026. Epub 2009 Apr 15.

Abstract

The effects of estrogen are widespread throughout the body. Although the classical nuclear estrogen receptors have been known for many years to decades and their primary modes of action as transcriptional regulators is well understood, certain aspects of estrogen biology remain inconsistent with the mechanisms of action of these receptor. More recently, the G protein-coupled receptor, GPR30/GPER, has been suggested to contribute to some of the cellular and physiological effects of estrogen. Not only does GPR30 mediate some of the rapid signal transduction events following cell stimulation, such as calcium mobilization and kinase activation, it also appears to regulate rapid transcriptional activation of genes such as c-fos. Since many cells and tissues co-express classical estrogen receptors and GPR30, there exists great diversity in the possible avenues of synergism and antagonism. In this review, we will provide an overview of GPR30 function, focusing on the rapid signaling events that culminate in the transcriptional activation of certain genes.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Estrogens / metabolism*
  • Gene Expression / physiology*
  • Humans
  • Receptors, Estrogen
  • Receptors, G-Protein-Coupled / metabolism*
  • Signal Transduction / physiology*
  • Transcriptional Activation*

Substances

  • Estrogens
  • GPER1 protein, human
  • Receptors, Estrogen
  • Receptors, G-Protein-Coupled