Evidence map›Paper›PMID 22495674›Full record

ReviewEndocrinology2012

Minireview: G protein-coupled estrogen receptor-1, GPER-1: its mechanism of action and role in female reproductive cancer, renal and vascular physiology.

Edward J Filardo, Peter Thomas

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Endocrinology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 190 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
190citing papers in PubMed, 1 pooled it
22.3field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

190 citing papers in PubMed, 1 synthesis or guideline pooled it, 355 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Overexpression of GPER1 suppressed esophageal carcinoma growthEuropean journal of histochemistry : EJH · 2026
    Article
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  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
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  14. Review
  15. The Role of Estrogen in Brain MicroRNAs Regulation.Advanced pharmaceutical bulletin · 2024
    Review
  16. Review
  17. Review
  18. Review
  19. Article
  20. Article

130 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

Edward J FilardoDepartment of Medicine, Rhode Island Hospital and Brown University Medical School, 593 Eddy Street, Aldrich Building Room 708, Providence, Rhode Island 02903, USA. edward_filardo@brown.edu
Peter Thomas
Rhode Island Hospital · USThe University of Texas at Austin · US

Funding

Study of GPR30: a novel estrogen receptor linked to breast cancer.R01CA119165 · NCI · RHODE ISLAND HOSPITAL · PI FILARDO, EDWARD J · 2007 to 2010
$1.2M
NCI NIH HHS R01 CA119165
6 · The paper itself

Abstract

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.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsBiopsyErbB ReceptorsFemaleGenital Neoplasms, FemaleHumansKidneyLigandsMiceModels, BiologicalModels, GeneticReceptors, EstrogenReceptors, G-Protein-CoupledTranscriptional ActivationErbB ReceptorsGPER1 protein, humanLigandsReceptors, EstrogenReceptors, G-Protein-Coupled

Identifiers

PMID22495674
PMCPMC3380306
OpenAlexW2137207319

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.