Evidence map›Paper›PMID 21736917›Full record

ReviewMolecular and cellular endocrinology2011

G protein-coupled receptors involved in GnRH regulation: molecular insights from human disease.

Sekoni D Noel, Ursula B Kaiser

Registry-linked trialAbstract readReview
In one paragraph

Review in Molecular and cellular endocrinology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02979886 (Effects of Single Nucleotide Polymorphism of GnRH Receptor Genes on Clinical Response to Pituitary Down Regulation in IVF Patients), which is not on this map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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.

NCT02979886 naunknown statusnot on this mapstarted 2017, after this paper: background citation

Effects of Single Nucleotide Polymorphism of GnRH Receptor Genes on Clinical Response to Pituitary Down Regulation in IVF Patients

TypeinterventionalSponsorMiao benyuRan2017 to 2019Enrolled1,500ConditionsInfertility, FemaleArmsGnRH-a, Human Menopausal Gonadotropins
3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Trafficking-defective mutant PROKR2 cycles between endoplasmic reticulum and Golgi to attenuate endoplasmic reticulum stress.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  5. Article
  6. Article
  7. Frontiers in genetics · 2018
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

Sekoni D NoelDivision of Endocrinology, Diabetes and Hypertension, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.
Ursula B Kaiser
Harvard University · US

Funding

The Genetic Determinants of Human GNRH DeficiencyU54HD028138 · NICHD · MASSACHUSETTS GENERAL HOSPITAL · PI CROWLEY, WILLIAM FRANCIS · 2000 to 2013
$19.9M
TRAINING GRANT IN ACADEMIC ENDOCRINOLOGYT32DK007529 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI Ursula B. Kaiser, Anand Vaidya · 1986 to 2026
$6.3M
THE NEUROENDOCRINE CONTROL OF REPRODUCTION IN THE HUMANR01HD015788 · NICHD · MASSACHUSETTS GENERAL HOSPITAL · PI CROWLEY, WILLIAM FRANCIS · 1985 to 2012
$4.6M
NICHD NIH HHS R01 HD015788NICHD NIH HHS U54 HD028138NICHD NIH HHS U54 HD28138NIDDK NIH HHS 5T32 DK007529-22
6 · The paper itself

Abstract

In the past two decades, an increasing body of evidence has demonstrated that several G protein-coupled receptor (GPCR)-ligand pairs are critical for normal human reproductive development and function. Patients harboring genetic insults in either the receptors or their cognate ligands have presented with reproductive disorders characterized by varying degrees of GnRH deficiency. These disorders include idiopathic hypogonadotropic hypogonadism (IHH) and Kallmann Syndrome (KS). Conversely, mutations in some of these ligand-receptor pairs have been associated with accelerated reproductive maturation, manifested as central precocious puberty (CPP). To date, a series of elegant studies have characterized four GPCRs that play important roles in the neuroendocrine control of human reproductive development and function: GnRHR, KISS1R, PROKR2 and NK3R. Furthermore, these studies provide insights into the mechanisms by which mutations in these receptors give rise to reproductive disease phenotypes. This report will review mutations identified in GPCRs involved in the neuroendocrine control of the human reproductive axis with the aims of elucidating structure-function relationships of these GPCRs and identifying correlations between these structure-function relationships and the genotypic-phenotypic characterization of the patients.

Indexed as

Gonadal DisordersGonadotropin-Releasing HormoneHumansMutationReceptors, G-Protein-CoupledReproductionGonadotropin-Releasing HormoneReceptors, G-Protein-Coupled

Identifiers

PMID21736917
PMCPMC3185177
OpenAlexW1997177607

What OpenQuestion holds

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Registered trials

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.