Evidence map›Paper›PMID 18511495›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2008

The Xenopus laevis isoform of G protein-coupled receptor 3 (GPR3) is a constitutively active cell surface receptor that participates in maintaining meiotic arrest in X. laevis oocytes.

James Deng, Stephanie Lang, Christopher Wylie, Stephen R Hammes

Open access · bronzeAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Regulation of oocyte maturation: Role of conserved ERK signaling.Molecular reproduction and development · 2022
    Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Dissection of the Ovulatory Process UsingFrontiers in cell and developmental biology · 2020
    Review
  12. Review
  13. The art of oocyte meiotic arrest regulation.Reproductive biology and endocrinology : RB&E · 2019
    Review
  14. Article
  15. Article
  16. Article
  17. Vertebrate Reproduction.Cold Spring Harbor perspectives in biology · 2015
    Review
  18. Overlapping nongenomic and genomic actions of thyroid hormone and steroids.Best practice & research. Clinical endocrinology & metabolism · 2015
    Review
  19. Paxillin and steroid signaling: from frog to human.Methods in molecular biology (Clifton, N.J.) · 2014
    Article
  20. Article
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

4 authors at 2 institutions in 1 country.

James DengDepartment of Internal Medicine, Division of Endocrinology and Metabolism, University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Boulevard, Dallas, Texas 75390, USA.
Stephanie Lang
Christopher Wylie
Stephen R Hammes
Cincinnati Children's Hospital Medical Center · USThe University of Texas Southwestern Medical Center · US

Funding

Nongenomic Steroid Signaling in OocytesR01DK059913 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI HAMMES, STEPHEN R. · 2002 to 2009
$2.8M
NIDDK NIH HHS DK59913NIDDK NIH HHS R01 DK059913
6 · The paper itself

Abstract

Oocytes are held in meiotic arrest in prophase I until ovulation, when gonadotropins trigger a subpopulation of oocytes to resume meiosis in a process termed "maturation." Meiotic arrest is maintained through a mechanism whereby constitutive cAMP production exceeds phosphodiesterase-mediated degradation, leading to elevated intracellular cAMP. Studies have implicated a constitutively activated Galpha(s)-coupled receptor, G protein-coupled receptor 3 (GPR3), as one of the molecules responsible for maintaining meiotic arrest in mouse oocytes. Here we characterized the signaling and functional properties of GPR3 using the more amenable model system of Xenopus laevis oocytes. We cloned the X. laevis isoform of GPR3 (XGPR3) from oocytes and showed that overexpressed XGPR3 elevated intraoocyte cAMP, in large part via Gbetagamma signaling. Overexpressed XGPR3 suppressed steroid-triggered kinase activation and maturation of isolated oocytes, as well as gonadotropin-induced maturation of follicle-enclosed oocytes. In contrast, depletion of XGPR3 using antisense oligodeoxynucleotides reduced intracellular cAMP levels and enhanced steroid- and gonadotropin-mediated oocyte maturation. Interestingly, collagenase treatment of Xenopus oocytes cleaved and inactivated cell surface XGPR3, which enhanced steroid-triggered oocyte maturation and activation of MAPK. In addition, human chorionic gonadotropin-treatment of follicle-enclosed oocytes triggered metalloproteinase-mediated cleavage of XGPR3 at the oocyte cell surface. Together, these results suggest that GPR3 moderates the oocyte response to maturation-promoting signals, and that gonadotropin-mediated activation of metalloproteinases may play a partial role in sensitizing oocytes for maturation by inactivating constitutive GPR3 signaling.

Indexed as

MeiosisAmino Acid SequenceAnimalsCell DifferentiationCell MembraneChorionic GonadotropinCloning, MolecularCollagenasesCyclic AMPFemaleHumansIntracellular SpaceModels, BiologicalMolecular Sequence DataOocytesOvarian FollicleChorionic GonadotropinCollagenasesCyclic AMPGPR3 protein, XenopusProtein IsoformsReceptors, G-Protein-CoupledTestosteroneXenopus Proteins

Identifiers

PMID18511495
PMCPMC2505325
OpenAlexW2040334419

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.