Journal
ANNUAL REVIEW OF PHYSIOLOGY
Volume 70, Issue -, Pages 165-190Publisher
ANNUAL REVIEWS
DOI: 10.1146/annurev.physiol.70.113006.100518
Keywords
estrogen receptor; steroid receptor; epidermal growth factor receptor
Categories
Funding
- NCI NIH HHS [P30 CA118100, CA118743, CA116662] Funding Source: Medline
- NIGMS NIH HHS [GM08136, GM068901] Funding Source: Medline
- NIMH NIH HHS [MH074425] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [P30CA118100, R01CA116662, R01CA118743] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM068901] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF MENTAL HEALTH [U54MH074425] Funding Source: NIH RePORTER
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Steroids play an important role in the regulation of normal physiology and the treatment of disease. Steroid receptors have classically been described as ligand-activated transcription factors mediating long-term genomic effects in hormonally regulated tissues. It is now clear that steroids also mediate rapid signaling events traditionally associated with growth factor receptors and G protein-coupled receptors. Although evidence suggests that the classical steroid receptors are capable of mediating many of these events, more recent discoveries reveal the existence of transmembrane receptors capable of responding to steroids with cellular activation. One such receptor, GPR30, is a member of the G protein-coupled receptor superfamily and mediates estrogen-dependent kinase activation as well as transcriptional responses. In this review, we provide an overview of the evidence for the cellular and physiological actions of GPR30 in estrogen-dependent processes and discuss the relationship of GPR30 with classical estrogen receptors.
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