Evidence map›Paper›PMID 28705934›Full record

ArticleThe Journal of biological chemistry2017

G

Rachit Badolia, Vaishali Inamdar, Bhanu Kanth Manne, Carol Dangelmaier, Johannes A Eble, Satya P Kunapuli

Open access · hybridAbstract readComparative Study
In one paragraph

Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

17 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Diverse innate stimuli activate basophils through pathways involving Syk and IκB kinases.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Heterotrimeric GThe Journal of biological chemistry · 2020
    Review
  14. TULA-2 Deficiency Enhances Platelet Functional Responses to CLEC-2 Agonists.TH open : companion journal to thrombosis and haemostasis · 2018
    Article
  15. Review
  16. Article
  17. 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

6 authors at 2 institutions in 2 countries.

Rachit BadoliaFrom the Department of Physiology.
Vaishali InamdarFrom the Department of Physiology.
Bhanu Kanth ManneFrom the Department of Physiology.
Carol DangelmaierFrom the Department of Physiology.
Johannes A Eblethe Institute of Physiological Chemistry and Pathobiochemistry, University of Münster, Waldeyerstrasse 15, 48149 Münster, Germany.
Satya P KunapuliFrom the Department of Physiology, spk@temple.edu.
Temple University · USUniversity of Münster · DE

Funding

Functional PKC Isoforms in PlateletsR01HL093231 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI KUNAPULI, SATYA P. · 2009 to 2017
$3.6M
Regulation and function of PDK1-Akt-Pyk2 axis in plateletsR01HL118593 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI KUNAPULI, SATYA P. · 2013 to 2016
$1.9M
Novel regulation of CLEC-2 signaling in PlateletsR01HL132171 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI KUNAPULI, SATYA P. · 2017 to 2020
$1.8M
NHLBI NIH HHS R01 HL093231NHLBI NIH HHS R01 HL118593NHLBI NIH HHS R01 HL132171
6 · The paper itself

Abstract

Platelets play a key role in the physiological hemostasis or pathological process of thrombosis. Rhodocytin, an agonist of the C-type lectin-like receptor-2 (CLEC-2), elicits powerful platelet activation signals in conjunction with Src family kinases (SFKs), spleen tyrosine kinase (Syk), and phospholipase γ2 (PLCγ2). Previous reports have shown that rhodocytin-induced platelet aggregation depends on secondary mediators such as thromboxane A2 (TxA2) and ADP, which are agonists for G-protein-coupled receptors (GPCRs) on platelets. How the secondary mediators regulate CLEC-2-mediated platelet activation in terms of signaling is not clearly defined. In this study, we report that CLEC-2-induced Syk and PLCγ2 phosphorylation is potentiated by TxA2 and that TxA2 plays a critical role in the most proximal event of CLEC-2 signaling,

Indexed as

Models, BiologicalSignal TransductionAnimalsBlood PlateletsCoagulantsDepsipeptidesEnzyme InhibitorsGTP-Binding Protein alpha Subunits, Gq-G11HumansLectins, C-TypeMice, KnockoutPhospholipase C gammaPhosphorylationPlatelet AggregationProtein Processing, Post-TranslationalProto-Oncogene Proteins c-fynCLEC1B protein, humanCoagulantsDepsipeptidesEnzyme InhibitorsFR900359Fyn protein, mouseGNAQ protein, humanGTP-Binding Protein alpha Subunits, Gq-G11Lectins, C-Typelyn protein-tyrosine kinasePhospholipase C gammaProto-Oncogene Proteins c-fynrhodocytin protein, Calloselasma rhodostomasrc-Family KinasesSyk KinaseSYK protein, humanThromboxane A2Viper Venomscell signalingCLEC-2 receptorG-protein-coupled receptor (GPCR)Gq signalingplateletplateletsrhodocytinsignal transductionsnake venom

Identifiers

PMID28705934
PMCPMC5582844
OpenAlexW2735089007

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.