Evidence map›Paper›PMID 26189910›Full record

ReviewThe Journal of steroid biochemistry and molecular biology2015

What have we learned about GPER function in physiology and disease from knockout mice?

Eric R Prossnitz, Helen J Hathaway

Open access · greenAbstract readReview
In one paragraph

Review in The Journal of steroid biochemistry and molecular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.

0numbers the graph read from it
0cells of the map it votes in
98citing papers in PubMed
12.1field-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

98 citing papers in PubMed, 151 citations in OpenAlex.

  1. Article
  2. Article
  3. Sexual dimorphism in the liver.Nature reviews. Gastroenterology & hepatology · 2026
    Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. GPER expression prevents estrogen-induced urinary retention in obese mice.The Journal of steroid biochemistry and molecular biology · 2024
    Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

38 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 1 institution in 1 country.

Eric R ProssnitzDepartment of Internal Medicine, University of New Mexico, Albuquerque, NM 87131, United States; University of New Mexico Cancer Center, Albuquerque, NM 87131, United States. Electronic address: eprossnitz@salud.unm.edu.
Helen J HathawayDepartment of Cell Biology & Physiology, University of New Mexico, Albuquerque, NM 87131, United States; University of New Mexico Cancer Center, Albuquerque, NM 87131, United States. Electronic address: hhathaway@salud.unm.edu.
University of New Mexico · US

Funding

WOMEN'S CANCERS RESEARCH PROGRAMP30CA118100 · NCI · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI Yolanda Sanchez · 2005 to 2026
$57.1M
UNM HSC Clinical and Translational Science CenterUL1TR001449 · NCATS · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI CAMPEN, MATTHEW J, PANDHI, NANCY · 2015 to 2024
$36.9M
G protein-coupled estrogen receptor GPER and breast carcinogenesisR01CA163890 · NCI · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI PROSSNITZ, ERIC R · 2012 to 2023
$3.3M
Development of GPR30-Selective LigandsR01CA127731 · NCI · UNIVERSITY OF NEW MEXICO · PI ARTERBURN, JEFFREY B, OPREA, TUDOR I · 2008 to 2012
$1.7M
A novel intracellular 7TM estrogen receptor in breastR01CA116662 · NCI · UNIVERSITY OF NEW MEXICO · PI PROSSNITZ, ERIC R · 2006 to 2010
$1.3M
The Role of GPR30 in Advanced Endometrial CancerR01CA118743 · NCI · UNIVERSITY OF NEW MEXICO · PI PROSSNITZ, ERIC R · 2007 to 2009
$855k
NCATS NIH HHS UL1 TR001449NCI NIH HHS P30 CA118100NCI NIH HHS R01 CA116662NCI NIH HHS R01 CA118743NCI NIH HHS R01 CA127731NCI NIH HHS R01 CA163890NCI NIH HHS R01 CA163890
6 · The paper itself

Abstract

Estrogens, predominantly 17β-estradiol, exert diverse effects throughout the body in both normal and pathophysiology, during development and in reproductive, metabolic, endocrine, cardiovascular, nervous, musculoskeletal and immune systems. Estrogen and its receptors also play important roles in carcinogenesis and therapy, particularly for breast cancer. In addition to the classical nuclear estrogen receptors (ERα and ERβ) that traditionally mediate predominantly genomic signaling, the G protein-coupled estrogen receptor GPER has become recognized as a critical mediator of rapid signaling in response to estrogen. Mouse models, and in particular knockout (KO) mice, represent an important approach to understand the functions of receptors in normal physiology and disease. Whereas ERα KO mice display multiple significant defects in reproduction and mammary gland development, ERβ KO phenotypes are more limited, and GPER KO exhibit no reproductive deficits. However, the study of GPER KO mice over the last six years has revealed that GPER deficiency results in multiple physiological alterations including obesity, cardiovascular dysfunction, insulin resistance and glucose intolerance. In addition, the lack of estrogen-mediated effects in numerous tissues of GPER KO mice, studied in vivo or ex vivo, including those of the cardiovascular, endocrine, nervous and immune systems, reveals GPER as a genuine mediator of estrogen action. Importantly, GPER KO mice have also demonstrated roles for GPER in breast carcinogenesis and metastasis. In combination with the supporting effects of GPER-selective ligands and GPER knockdown approaches, GPER KO mice demonstrate the therapeutic potential of targeting GPER activity in diseases as diverse as obesity, diabetes, multiple sclerosis, hypertension, atherosclerosis, myocardial infarction, stroke and cancer.

Indexed as

AnimalsCardiovascular DiseasesDiabetes MellitusDisease Models, AnimalHumansImmunityMiceMice, KnockoutNeoplasmsObesityReceptors, EstrogenReceptors, G-Protein-CoupledReceptors, EstrogenReceptors, G-Protein-CoupledCancerCardiovascularDiabetesEstrogenImmuneMetabolismObesityReceptors

Identifiers

PMID26189910
PMCPMC4568147
OpenAlexW923732998

What OpenQuestion holds

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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.