Evidence map›Paper›PMID 23502766›Full record

ArticleJournal of immunotherapy (Hagerstown, Md. : 1997)2013

The G protein-coupled estrogen receptor (GPER) agonist G-1 expands the regulatory T-cell population under TH17-polarizing conditions.

Ryan L Brunsing, Kristin S Owens, Eric R Prossnitz

Open access · greenAbstract read
In one paragraph

Article in Journal of immunotherapy (Hagerstown, Md. : 1997), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

36 citing papers in PubMed, 67 citations in OpenAlex.

  1. Article
  2. GPER expression prevents estrogen-induced urinary retention in obese mice.The Journal of steroid biochemistry and molecular biology · 2024
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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

3 authors at 1 institution in 1 country.

Ryan L BrunsingDepartment of Cell Biology and Physiology, University of New Mexico Health Science Center, Albuquerque, NM 87131, USA.
Kristin S Owens
Eric R Prossnitz
University of New Mexico · US

Funding

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
UNM Initiative to Maximize Student Diversity (IMSD)R25GM060201 · NIGMS · UNIVERSITY OF NEW MEXICO · PI WERNER-WASHBURNE, MARGRET C. · 2000 to 2017
$9.9M
University of New Mexico Clinical and Translational Science CenterUL1TR000041 · NCATS · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI LARSON, RICHARD S · 2012 to 2014
$9.8M
Biology of Infectious Diseases &InflammationT32AI007538 · NIAID · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI Michelle A Ozbun · 1998 to 2026
$5.2M
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 TR000041NCATS NIH HHS UL1 TR001449NCI NIH HHS CA118743NCI NIH HHS CA127731NCI NIH HHS CA163890NCI NIH HHS R01 CA116662NCI NIH HHS R01 CA127731NCI NIH HHS R01 CA163890NIAID NIH HHS T32 AI007538NIGMS NIH HHS R25 GM060201
6 · The paper itself

Abstract

The transcription factor Foxp3 is critical to the suppressive phenotype of CD4+ regulatory T cells. Studies have clearly shown that numerous autoimmune diseases are marked by the presence of activated CD4+ T cells within the setting of chronic inflammation. Therefore, drugs capable of inducing Foxp3 expression in activated CD4+ T cells could be of great therapeutic interest. We have previously shown that the small molecule G-1, an agonist directed against the membrane-bound G protein-coupled estrogen receptor, can induce IL10 expression in naive CD4+ T cells. In addition, we and others have demonstrated that G-1 attenuates disease in an animal model of experimental autoimmune encephalomyelitis. Using ex vivo cultures of purified CD4+ T cells, we show that G-1 can elicit Foxp3 expression under TH17-polarizing conditions, which mimic the in situ inflammatory milieu of several autoimmune diseases. These findings build upon previous results demonstrating the immunosuppressive properties of the novel estrogenic small molecule G-1.

Indexed as

AnimalsCell DifferentiationCells, CulturedCyclopentanesEncephalomyelitis, Autoimmune, ExperimentalForkhead Transcription FactorsLymphocyte ActivationMiceMice, Inbred C57BLQuinolinesReceptors, EstrogenReceptors, G-Protein-CoupledRNA, MessengerTh17 CellsT-Lymphocytes, Regulatory1-(4-(6-bromobenzo(1,3)dioxol-5-yl)-3a,4,5,9b-tetrahydro-3H-cyclopenta(c)quinolin-8-yl)ethanoneCyclopentanesForkhead Transcription FactorsFoxp3 protein, mouseGPER1 protein, mouseQuinolinesReceptors, EstrogenReceptors, G-Protein-CoupledRNA, Messenger

Identifiers

PMID23502766
PMCPMC3635139
OpenAlexW2004512161

What OpenQuestion holds

Textmetadata
LicenceTDM
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.