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Unless otherwise stated all data on this page refer to the human proteins. Gene information is provided for human (Hs), mouse (Mm) and rat (Rn).
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Estrogen receptor (ER) activity regulates diverse physiological processes via transcriptional modulation of target genes [1]. The selection of target genes and the magnitude of the response, be it induction or repression, are determined by many factors, including the effect of the hormone ligand and DNA binding on ER structural conformation, and the local cellular regulatory environment. The cellular environment defines the specific complement of DNA enhancer and promoter elements present and the availability of coregulators to form functional transcription complexes. Together, these determinants control the resulting biological response.
Estrogen receptor-α / NR3A1 C Show summary » More detailed page |
Estrogen receptor-β / NR3A2 C Show summary » More detailed page |
Database page citation (select format):
Concise Guide to PHARMACOLOGY citation:
Alexander SPH, Cidlowski JA, Kelly E, Mathie AA, Peters JA, Veale EL, Armstrong JF, Faccenda E, Harding SD, Davies JA et al. (2023) The Concise Guide to PHARMACOLOGY 2023/24: Nuclear hormone receptors. Br J Pharmacol. 180 Suppl 2:S223-240.
R,R-THC exhibits partial agonist activity at ERα [8,14]. Estrogen receptors may be blocked non-selectively by tamoxifen and raloxifene and labelled by [3H]17β-estradiol and [3H]tamoxifen. Many agents thought initially to be antagonists at estrogen receptors appear to have tissue-specific efficacy (e.g. Tamoxifen is an antagonist at estrogen receptors in the breast, but is an agonist at estrogen receptors in the uterus), hence the descriptor SERM (selective estrogen receptor modulator) or SnuRM (selective nuclear receptor modulator). Y134 has been suggested to be an ERα-selective estrogen receptor modulator [11].