Evidence map›Paper›PMID 23489111›Full record

ReviewBritish journal of pharmacology2013

Discriminating between 5-HT₃A and 5-HT₃AB receptors.

A J Thompson, S C R Lummis

Abstract readComparative StudyReview
In one paragraph

Review in British journal of pharmacology, 2013. 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. Article
  3. Review
  4. Article
  5. Predicted conformations of 5-HT3 receptor ion channels are modified by subunit D.Computational and structural biotechnology journal · 2025
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Tapping into 5-HTInternational journal of molecular sciences · 2021
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Human-derived gut microbiota modulates colonic secretion in mice by regulating 5-HTAmerican journal of physiology. Gastrointestinal and liver physiology · 2017
    Article
  19. 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

2 authors.

A J ThompsonDepartment of Biochemistry, University of Cambridge, Cambridge, UK. ajt44@cam.ac.uk
S C R Lummis

Funding

Wellcome TrustWellcome Trust 81295
6 · The paper itself

Abstract

The 5-HT3B subunit was first cloned in 1999, and co-expression with the 5-HT3A subunit results in heteromeric 5-HT₃AB receptors that are functionally distinct from homomeric 5-HT₃A receptors. The affinities of competitive ligands at the two receptor subtypes are usually similar, but those of non-competitive antagonists that bind in the pore often differ. A competitive ligand and allosteric modulator that distinguishes 5-HT₃A from 5-HT₃AB receptors has recently been described, and the number of non-competitive antagonists identified with this ability has increased in recent years. In this review, we discuss the differences between 5-HT₃A and 5-HT₃AB receptors and describe the possible sites of action of compounds that can distinguish between them.

Indexed as

Models, MolecularAllosteric RegulationAnimalsAntiemeticsBinding, CompetitiveBinding SitesDrug Partial AgonismHumansLigandsMolecular ConformationProtein MultimerizationProtein SubunitsReceptors, Serotonin, 5-HT3Recombinant ProteinsSerotonin 5-HT3 Receptor AgonistsSerotonin 5-HT3 Receptor AntagonistsAntiemeticsHTR3A protein, humanHTR3B protein, humanLigandsProtein SubunitsReceptors, Serotonin, 5-HT3Recombinant ProteinsSerotonin 5-HT3 Receptor AgonistsSerotonin 5-HT3 Receptor Antagonists

Identifiers

PMID23489111
PMCPMC3687655

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.