Evidence map›Paper›PMID 30930853›Full record

ReviewFrontiers in endocrinology2019

Biased Signaling and Allosteric Modulation at the FSHR.

Flavie Landomiel, Francesco De Pascali, Pauline Raynaud, Frédéric Jean-Alphonse, Romain Yvinec, Lucie P Pellissier, Véronique Bozon, Gilles Bruneau, Pascale Crépieux, Anne Poupon and 1 more

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in endocrinology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

26 citing papers in PubMed, 45 citations in OpenAlex.

  1. Trial
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  13. Allosteric modulation of gonadotropin receptors.Frontiers in endocrinology · 2023
    Review
  14. Article
  15. Article
  16. Review
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  18. Novel allosteric ligands of the angiotensin receptor AT1R as autoantibody blockers.Proceedings of the National Academy of Sciences of the United States of America · 2021
    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

11 authors at 3 institutions in 1 country.

Flavie LandomielPRC, INRA, CNRS, IFCE, Université de Tours, Nouzilly, France.
Francesco De PascaliPRC, INRA, CNRS, IFCE, Université de Tours, Nouzilly, France.
Pauline RaynaudPRC, INRA, CNRS, IFCE, Université de Tours, Nouzilly, France.
Frédéric Jean-AlphonsePRC, INRA, CNRS, IFCE, Université de Tours, Nouzilly, France.
Romain YvinecPRC, INRA, CNRS, IFCE, Université de Tours, Nouzilly, France.
Lucie P PellissierPRC, INRA, CNRS, IFCE, Université de Tours, Nouzilly, France.
Véronique BozonPRC, INRA, CNRS, IFCE, Université de Tours, Nouzilly, France.
Gilles BruneauPRC, INRA, CNRS, IFCE, Université de Tours, Nouzilly, France.
Pascale CrépieuxPRC, INRA, CNRS, IFCE, Université de Tours, Nouzilly, France.
Anne PouponPRC, INRA, CNRS, IFCE, Université de Tours, Nouzilly, France.
Eric ReiterPRC, INRA, CNRS, IFCE, Université de Tours, Nouzilly, France.
Centre National de la Recherche Scientifique · FRPhysiologie de la Reproduction et des Comportements · FRUniversité de Tours · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Knowledge on G protein-coupled receptor (GPCRs) structure and mechanism of activation has profoundly evolved over the past years. The way drugs targeting this family of receptors are discovered and used has also changed. Ligands appear to bind a growing number of GPCRs in a competitive or allosteric manner to elicit balanced signaling or biased signaling (i.e., differential efficacy in activating or inhibiting selective signaling pathway(s) compared to the reference ligand). These novel concepts and developments transform our understanding of the follicle-stimulating hormone (FSH) receptor (FSHR) biology and the way it could be pharmacologically modulated in the future. The FSHR is expressed in somatic cells of the gonads and plays a major role in reproduction. When compared to classical GPCRs, the FSHR exhibits intrinsic peculiarities, such as a very large NH2-terminal extracellular domain that binds a naturally heterogeneous, large heterodimeric glycoprotein, namely FSH. Once activated, the FSHR couples to Gαs and, in some instances, to other Gα subunits. G protein-coupled receptor kinases and β-arrestins are also recruited to this receptor and account for its desensitization, trafficking, and intracellular signaling. Different classes of pharmacological tools capable of biasing FSHR signaling have been reported and open promising prospects both in basic research and for therapeutic applications. Here we provide an updated review of the most salient peculiarities of FSHR signaling and its selective modulation.

Indexed as

biasfollicle-stimulating hormoneGPCRG proteinreproductionsignalingtraffickingβ-arrestin

Identifiers

PMID30930853
PMCPMC6425863
OpenAlexW2921051332

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.