Evidence map›Paper›PMID 21718310›Full record

ReviewBritish journal of pharmacology2012

Consequences of splice variation on Secretin family G protein-coupled receptor function.

Sebastian G B Furness, Denise Wootten, Arthur Christopoulos, Patrick M Sexton

Abstract readReview
In one paragraph

Review in British journal of pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
–field-weighted citation impact
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. Review
  2. Molecular basis of signal transduction mediated by the human GIPR splice variants.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  3. Calcitonin/PACTrends in pharmacological sciences · 2023
    Review
  4. Review
  5. PACInternational journal of molecular sciences · 2022
    Article
  6. Lighting up Nobel Prize-winning studies with protein intrinsic disorder.Cellular and molecular life sciences : CMLS · 2022
    Review
  7. Review
  8. Review
  9. Constitutive signal bias mediated by the human GHRHR splice variant 1.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. Review
  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.

Sebastian G B FurnessDepartment of Pharmacology, Monash University, Parkville, Victoria, Australia. sebastian.furness@monash.edu
Denise Wootten
Arthur Christopoulos
Patrick M Sexton

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Secretin family of GPCRs are endocrine peptide hormone receptors that share a common genomic organization and are the subject of a wide variety of alternative splicing. All GPCRs contain a central seven transmembrane domain responsible for transducing signals from the outside of the cell as well as extracellular amino and intracellular carboxyl termini. Members of the Secretin receptor family have a relatively large N-terminus and a variety of lines of evidence support a common mode of ligand binding and a common ligand binding fold. These receptors are best characterized as coupling to intracellular signalling pathways via G(αs) and G(αq) but are also reported to couple to a multitude of other signalling pathways. The intracellular loops are implicated in regulating the interaction between the receptor and heterotrimeric G protein complexes. Alternative splicing of exons encoding both the extracellular N-terminal domain as well as the extracellular loops of some family members has been reported and as expected these splice variants display altered ligand affinity as well as differential activation by endogenous ligands. Various forms of alternative splicing have also been reported to alter intracellular loops 1 and 3 as well as the C-terminus and as one might expect these display differences in signalling bias towards downstream effectors. These diverse pharmacologies require that the physiological role of these splice variants be addressed but should provide unique opportunities for drug design and development.

Indexed as

Alternative SplicingAnimalsDrug DesignHumansLigandsProtein BindingReceptors, Gastrointestinal HormoneReceptors, G-Protein-CoupledSignal TransductionLigandsReceptors, Gastrointestinal HormoneReceptors, G-Protein-Coupledsecretin receptor

Identifiers

PMID21718310
PMCPMC3415641

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.