Evidence map›Paper›PMID 25619861›Full record

ArticleMolecular and cellular endocrinology2015

GnRH agonist reduces estrogen receptor dimerization in GT1-7 cells: evidence for cross-talk between membrane-initiated estrogen and GnRH signaling.

Rebecca J Chason, Jung-Hoon Kang, Sabrina A Gerkowicz, Maria L Dufau, Kevin J Catt, James H Segars

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular and cellular endocrinology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
3.0field-weighted citation impact, top 10% 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

3 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
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

6 authors at 2 institutions in 1 country.

Rebecca J ChasonProgram in Reproductive and Adult Endocrinology, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, 10 CRC, Room 1E-3140, 10 Center Drive, MSC 1109, Bethesda, MD 20892-1109, USA.
Jung-Hoon KangSection on Molecular Endocrinology, Program on Developmental Endocrinology and Genetics, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892-4510, USA.
Sabrina A GerkowiczDepartment of Obstetrics and Gynecology, University of Miami, 1611 NW 12th Ave, Miami, FL 33136, USA.
Maria L DufauSection on Molecular Endocrinology, Program on Developmental Endocrinology and Genetics, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892-4510, USA.
Kevin J CattEndocrinology and Reproduction Research Branch, Section on Hormonal Regulation, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, USA.
James H SegarsProgram in Reproductive and Adult Endocrinology, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, 10 CRC, Room 1E-3140, 10 Center Drive, MSC 1109, Bethesda, MD 20892-1109, USA. Electronic address: segarsj@mail.nih.gov.
National Institutes of Health · USUniversity of Miami · US

Funding

Regulation of Hormone Receptors and Gonadal GenesZIAHD000150 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI DUFAU, MARIA · 2009 to 2022
$15.9M
Reproductive Endocrinology And Infertility Clinical Training ProgramZIAHD008737 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI SEGARS, JAMES H. · 2009 to 2010
$3.2M
Reproductive Endocrinology And Infertility TrainingZ01HD008737 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI SEGARS, JAMES H. · 2001 to 2008
$2.7M
Regulation of the Hypothalamic GnRH NeuronZ01HD000184 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI CATT, KEVIN J · 1985 to 2008
$1.7M
Intramural NIH HHS Z01 HD000184Intramural NIH HHS Z01 HD008737Intramural NIH HHS ZIA HD000150Intramural NIH HHS ZIA HD008737NICHD NIH HHS Z01-HD 008737NICHD NIH HHS ZIA-HD 000150-39
6 · The paper itself

Abstract

17β-estradiol (E2), a key participant on the initiation of the LH surge, exerts both positive and negative feedback on GnRH neurons. We sought to investigate potential interactions between estrogen receptors alpha (ERα) and beta (ERβ) and gonadotropin releasing hormone receptor (GnRH-R) in GT1-7 cells. Radioligand binding studies demonstrated a significant decrease in saturation E2 binding in cells treated with GnRH agonist. Conversely, there was a significant reduction in GnRH binding in GT1-7 cells treated with E2. In BRET(1) experiments, ERα-ERα dimerization was suppressed in GT1-7 cells treated with GnRH agonist (p < 0.05). There was no evidence of direct interaction between ERs and GnRH-R. This study provides the first evidence of reduced ERα homodimerization by GnRH agonist. Collectively, these findings demonstrate significant cross-talk between membrane-initiated GnRH and E2 signaling in GT1-7 cells.

Indexed as

Signal TransductionBinding SitesBioluminescence Resonance Energy Transfer TechniquesCell LineEstradiolEstrogen Receptor alphaEstrogen Receptor betaGonadotropin-Releasing HormoneHEK293 CellsHumansNeuronsProtein MultimerizationRadioligand AssayEstradiolEstrogen Receptor alphaEstrogen Receptor betaGonadotropin-Releasing HormoneEstradiolEstrogen receptor alphaEstrogen receptor betaGnRH receptorGT1-7 cellsNon-classical estrogen signaling

Identifiers

PMID25619861
PMCPMC4590284
OpenAlexW1965653369

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.