Evidence map›Paper›PMID 8968535›Full record

ArticleBritish journal of pharmacology1996

Cloned and transfected P2Y4 receptors: characterization of a suramin and PPADS-insensitive response to UTP.

S J Charlton, C A Brown, G A Weisman, J T Turner, L Erb, M R Boarder

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

19 citing papers in PubMed, 89 citations in OpenAlex.

  1. Advances in nucleotide-based P2Y₁ antagonism: implications for cardiovascular therapeutics.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2026
    Review
  2. P2YFrontiers in immunology · 2023
    Article
  3. P2YInternational journal of molecular sciences · 2020
    Article
  4. Article
  5. P2Y2 receptors mediate ATP-induced resensitization of TRPV1 expressed by kidney projecting sensory neurons.American journal of physiology. Regulatory, integrative and comparative physiology · 2010
    Article
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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

6 authors at 1 institution in 1 country.

S J CharltonDepartment of Cell Physiology and Pharmacology, University of Leicester.
C A Brown
G A Weisman
J T Turner
L Erb
M R Boarder
University of Leicester · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

The P2Y family of receptors are G protein-coupled receptors for ATP, ADP, UTP and UDP. Recently several members of this family have been cloned, including the P2Y4, which is activated by UTP but not by ATP. In the present report, using receptors stably transfected into 1321N1 cells, we show that suramin acts as an antagonist at cloned P2Y1 and (less potently) P2Y2 receptors, but not at the cloned P2Y4 receptor. Furthermore, PPADS (pyridoxal-phosphate-6-azophenyl-2',4'-disulphonic acid), a potent antagonist at the P2Y1 receptor, is a relatively inneffective antagonist at the cloned P2Y4 receptor. This work moves us closer to the goal of classifying the native P2Y receptors on the basis of agonist and antagonist profiles.

Indexed as

Purinergic P2 Receptor AntagonistsCell LineCloning, MolecularHumansPyridoxal PhosphateReceptors, Purinergic P2SuraminTransfectionUridine TriphosphatePurinergic P2 Receptor Antagonistspurinoceptor P2Y4Pyridoxal Phosphatepyridoxal phosphate-6-azophenyl-2',4'-disulfonic acidReceptors, Purinergic P2SuraminUridine Triphosphate

Identifiers

PMID8968535
PMCPMC1915815
OpenAlexW2073946901

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.