Estrogen receptors and human disease
Bonnie J. Deroo, Kenneth S. Korach
Bonnie J. Deroo, Kenneth S. Korach
Published March 1, 2006
Citation Information: J Clin Invest. 2006;116(3):561-570. https://doi.org/10.1172/JCI27987.
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Estrogen receptors and human disease

Abstract

Estrogens influence many physiological processes in mammals, including but not limited to reproduction, cardiovascular health, bone integrity, cognition, and behavior. Given this widespread role for estrogen in human physiology, it is not surprising that estrogen is also implicated in the development or progression of numerous diseases, which include but are not limited to various types of cancer (breast, ovarian, colorectal, prostate, endometrial), osteoporosis, neurodegenerative diseases, cardiovascular disease, insulin resistance, lupus erythematosus, endometriosis, and obesity. In many of these diseases, estrogen mediates its effects through the estrogen receptor (ER), which serves as the basis for many therapeutic interventions. This Review will describe diseases in which estrogen, through the ER, plays a role in the development or severity of disease.

Authors

Bonnie J. Deroo, Kenneth S. Korach

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Differential ER structure and coactivator recruitment by ER agonists, an...
Differential ER structure and coactivator recruitment by ER agonists, antagonists, and SERMs. Upon binding ER ligands such as estradiol or SERMs, the receptor undergoes a conformational change, allowing the ER to exist in a spectrum of conformations from active to inactive depending on the nature of the bound ligand. This conformation, in turn, regulates the recruitment of specific transcriptional coregulatory proteins and the resulting transcriptional apparatus. Coactivators such as SRC1 bind to the active (agonist-bound) form of the receptor and activate transcription, while corepressors interact with the antagonist-bound receptor, inhibiting transcription. Depending on the cellular and promoter context, both unique and overlapping sets of genes may be regulated by various ligands. Adapted with permission from The American Journal of Cardiology (S35).