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. Author manuscript; available in PMC: 2024 Dec 1.
Published in final edited form as: Laryngoscope. 2023 Jun 29;133(12):3506–3511. doi: 10.1002/lary.30856

Figure 1. Estrogen and progesterone signaling.

Figure 1.

(A)17β-estradiol is the natural estrogen receptor (ER) agonist and can bind to either ER alpha (ERα) or beta (ERβ). Estrogen-mediated direct genomic signaling involves hormone binding to estrogen receptors in the cytosol, leading to homo/hetero dimerization (ERα:ERα / ERα:ERβ / ERβ:ERβ). The ER dimers then translocate to the nucleus and bind to the DNA on the regulatory regions of estrogen-responsive genes. Estrogen can also activate a membrane bound G protein-coupled estrogen receptor (GPER1), which initiates rapid intracellular signaling cascades such as adenylyl cyclase/cAMP and EGFR/MAPK. Both the nuclear receptors (ERα & ERβ) and GPER1 can modulate nongenomic signaling pathways. (B) Progesterone’s effects are primarily transduced through ligand binding to progesterone receptors (PR) in the cytosol. Ligand-bound complexes dimerize and translocate to the nucleus where they bind to gene regulatory regions including progesterone response elements (PREs) to initiate transcription of progesterone-responsive genes. Progesterone can also exert nongenomic effects via binding to a membrane progesterone receptor (mPR).