Evidence map›Paper›PMID 9653141›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1998

Coactivation of two different G protein-coupled receptors is essential for ADP-induced platelet aggregation.

J Jin, S P Kunapuli

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 149 papers.

0numbers the graph read from it
0cells of the map it votes in
149citing papers in PubMed
17.4field-weighted citation impact, top 1% 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

149 citing papers in PubMed, 537 citations in OpenAlex.

  1. Article
  2. Review
  3. Selective Inhibition of Integrin β3 Topology Provides a Safer Antithrombotic Strategy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  4. Article
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  7. Antiplatelet Therapy.Handbook of experimental pharmacology · 2026
    Review
  8. Purinergic P2YPurinergic signalling · 2025
    Article
  9. Design and Pharmacological Characterization of a Novel Antithrombotic P2YInternational journal of molecular sciences · 2025
    Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Exploring bias in platelet P2YBritish journal of pharmacology · 2024
    Review
  15. Article
  16. Review
  17. Role of Prednisolone in Platelet Activation by Inhibiting TxAAnimals : an open access journal from MDPI · 2023
    Article
  18. Antiplatelet Effect of Daphnetin Is Regulated by cPLAInternational journal of molecular sciences · 2023
    Article
  19. Platelet P2YBMC biology · 2023
    Article
  20. Article

89 more citing papers are in PubMed but not listed here.

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 at 1 institution in 1 country.

J JinDepartment of Physiology, Temple University Medical School, Philadelphia, PA 19140, USA.
S P Kunapuli
Temple University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

ADP is an important platelet agonist causing shape change and aggregation required for physiological hemostasis. We recently demonstrated the existence of two distinct G protein-coupled ADP receptors on platelets, one coupled to phospholipase C, P2Y1, and the other to inhibition of adenylyl cyclase, P2TAC. In this study, using specific antagonists for these two receptors, we demonstrated that concomitant intracellular signaling from both the P2TAC and P2Y1 receptors is essential for ADP-induced platelet aggregation. Inhibition of signaling through either receptor, by specific antagonists, is sufficient to block ADP-induced platelet aggregation. Furthermore, signaling through the P2TAC receptor could be replaced by activation of alpha2A-adrenergic receptors. On the other hand, activation of serotonin receptors supplements signaling through the P2Y1 receptor. Moreover, this mechanism of ADP-induced platelet aggregation could be mimicked by coactivation of two non-ADP receptors coupled to Gi and Gq, neither of which can cause platelet aggregation by itself. We propose that platelet aggregation results from concomitant signaling from both the Gi and Gq, a mechanism by which G protein-coupled receptors elicit a physiological response.

Indexed as

Platelet AggregationAdenosine DiphosphateElectrophysiologyGTP-Binding ProteinsHumansPurinergic P2 Receptor AgonistsReceptors, Purinergic P2Signal TransductionAdenosine DiphosphateGTP-Binding ProteinsPurinergic P2 Receptor AgonistsReceptors, Purinergic P2

Identifiers

PMID9653141
PMCPMC20930
OpenAlexW2016217548

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.