Estrogen receptor; Progesterone receptor (ER; PR)

Estrogen receptor (ER) and progesterone receptor (PR) are members of the nuclear receptor superfamily of ligand-dependent transcription factors, critical to the regulation of gene transcription in response to their respective steroid hormones, estrogen and progesterone[1][4][6]. ER exists primarily as two isoforms—ER alpha (ESR1) and ER beta (ESR2)—and mediates diverse physiological effects in reproductive tissues (e.g., breast, uterus, ovary), bone, cardiovascular, and nervous systems[4][2]. Progesterone receptor also has two main isoforms, PRA and PRB, which modulate transcriptional programs involved in reproduction, pregnancy, and hormone-dependent tumor biology[6]. Both ER and PR serve as important therapeutic targets in hormone-dependent cancers, especially breast and gynecological cancers[8]. Drugs targeting these receptors exploit their ligand binding domains, functioning as agonists, antagonists, or selective modulators (such as SERMs for ER)[3][4]. Expression of ER and PR in tumors is routinely used as a biomarker to determine suitability for endocrine therapies and as a prognostic factor in oncology[4][8]. Note: The entry "Estrogen and Progesterone Receptors" is not a single molecular entity but rather refers to two distinct, though related, nuclear receptors; structured information should thus be obtained separately for each receptor (ER, PR)[4][1].

Other names

Estrogen receptor alpha (ERα)Estrogen receptor beta (ERβ)G protein-coupled estrogen receptor 1 (GPER1)Progesterone receptor A (PRA)Progesterone receptor B (PRB)Nuclear estrogen receptorNuclear progesterone receptor

Agonism (mimic endogenous ligand to activate receptor); Antagonism (block endogenous hormone binding and activity); Selective modulation (different tissue-specific activation or inhibition, e.g., SERMs for ER); Downregulation/degradation (e.g., selective estrogen receptor degrader/antagonist)