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Minireview: G Protein-Coupled Estrogen Receptor-1, GPER-1: Its Mechanism of Action and Role in Female Reproductive Cancer, Renal and Vascular Physiology
Open accessAbstract
Using cDNA cloning strategies commonly employed for G protein-coupled receptors (GPCR), GPCR-30 (GPR30), was isolated from mammalian cells before knowledge of its cognate ligand. GPR30 is evolutionarily conserved throughout the vertebrates. A broad literature suggests that GPR30 is a Gs-coupled heptahelical transmembrane receptor that promotes specific binding of naturally occurring and man-made estrogens but not cortisol, progesterone, or testosterone. Its “pregenomic” signaling actions are manifested by plasma membrane-associated actions familiar to GPCR, namely, stimulation of adenylyl cyclase and Gβγ-subunit protein-dependent release of membrane-tethered heparan bound epidermal growth factor. These facts regarding its mechanism of action have led to the formal renaming of this receptor to its current functional designate, G protein-coupled estrogen receptor (ER) (GPER)-1. Further insight regarding its biochemical action and physiological functions in vertebrates is derived from receptor knockdown studies and the use of selective agonists/antagonists that discriminate GPER-1 from the nuclear steroid hormone receptors, ERα and ERβ. GPER-1-selective agents have linked GPER-1 to physiological and pathological events regulated by estrogen action, including, but not limited to, the central nervous, immune, renal, reproductive, and cardiovascular systems. Moreover, immunohistochemical studies have shown a positive association between GPER-1 expression and progression of female reproductive cancer, a relationship that is diametrically opposed from ER. Unlike ER knockout mice, GPER-1 knockout mice are fertile and show no overt reproductive anomalies. However, they do exhibit thymic atrophy, impaired glucose tolerance, and altered bone growth. Here, we discuss the role of GPER-1 in female reproductive cancers as well as renal and vascular physiology.
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“Estrogen transmits signals via GPERs to transactivate epidermal growth factor receptors for cell proliferation in female reproductive cancers [26].”
From G protein-coupled receptors function as cell membrane receptors for the steroid hormone 20-hydroxyecdysone (2020) · cites this paper as [26]
In the citing paper
“GPER1-mediated nongenomic activity is independent of the estrogen nuclear receptor [26].”
From G protein-coupled receptors function as cell membrane receptors for the steroid hormone 20-hydroxyecdysone (2020) · cites this paper as [26]
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“GPR30 has shown negligible binding to estrogen (17β-estradiol) in several studies [49], which may be due to the different analytical methods [17].”
From G-protein-coupled receptor participates in 20-hydroxyecdysone signaling on the plasma membrane (2014) · cites this paper as [17]
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Metadata
- Authors
- Filardo, E. J., & Thomas, P.
- Affiliations
- Brown University (US)
- University of Texas at Austin Marine Science Institute (US)
- Corresponding author
- Filardo, Edward J.
- Venue
- Endocrinology
- Publisher
- The Endocrine Society
- Published
- 2012-04-11
- Volume
- 153
- Issue
- 7
- Pages
- 2953-2962
- ISSN
- 0013-7227 (ISSN-L)
- 1945-7170
- PMC
- PMC3380306
- OpenAlex
- W2137207319
- Cited by
- 366
- References
- 83
- Citations by year
- 2026: 16 · 2025: 10 · 2024: 24 · 2023: 16 · 2022: 18 · 2021: 28 · 2020: 31 · 2019: 30 · 2018: 29 · 2017: 26 · 2016: 28 · 2015: 36 · 2014: 36 · 2013: 29 · 2012: 9
- FWCI
- 4.34
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Endocrinology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Cancer Institute (R01CA119165)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Endocrinology › Estrogen and related hormone effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Receptor Mechanisms and Signaling
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Effects and risks of endocrine disrupting chemicals
- Keywords
- G protein-coupled estrogen receptor, GPR30, estrogen signaling, female reproductive cancers, renal physiology, vascular physiology, adenylate cyclase, Gβγ subunits, estrogen receptor knockout mice, thymic atrophy, glucose tolerance, bone growth
- MeSH terms
- Animals, Biopsy, Female, Genital Neoplasms, Female, Humans, Kidney, Ligands, Models, Biological, Models, Genetic, Receptors, Estrogen, Transcriptional Activation, Gene Expression Regulation, Neoplastic, Receptors, G-Protein-Coupled, Mice, ErbB Receptors
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