Evidence map›Paper›PMID 28719611›Full record

ArticlePloS one2017

RNA sequencing to determine the contribution of kinase receptor transactivation to G protein coupled receptor signalling in vascular smooth muscle cells.

Danielle Kamato, Venkata Vijayanand Bhaskarala, Nitin Mantri, Tae Gyu Oh, Dora Ling, Reearna Janke, Wenhua Zheng, Peter J Little, Narin Osman

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

10 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Article
  3. Diversification of PAR signaling through receptor crosstalk.Cellular & molecular biology letters · 2022
    Review
  4. Article
  5. Article
  6. A cellular perspective of bias at G protein-coupled receptors.Protein science : a publication of the Protein Society · 2020
    Review
  7. Review
  8. Article
  9. Review
  10. The Role of G Protein-coupled Receptor Kinases in Cancer.International journal of biological sciences · 2018
    Review
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

9 authors at 4 institutions in 3 countries.

Danielle KamatoSchool of Pharmacy, The University of Queensland, Pharmacy Australia Centre of Excellence, Woolloongabba, QLD, Australia.ORCID http://orcid.org/0000-0002-1089-2829
Venkata Vijayanand BhaskaralaDepartment of Biotechnology and Environmental Biology, School of Applied Sciences, RMIT University, Bundoora, VIC, Australia.
Nitin MantriDepartment of Biotechnology and Environmental Biology, School of Applied Sciences, RMIT University, Bundoora, VIC, Australia.
Tae Gyu OhInstitute for Molecular Bioscience, The University of Queensland, St Lucia, Qld, Australia.
Dora LingSchool of Pharmacy, The University of Queensland, Pharmacy Australia Centre of Excellence, Woolloongabba, QLD, Australia.
Reearna JankeSchool of Pharmacy, The University of Queensland, Pharmacy Australia Centre of Excellence, Woolloongabba, QLD, Australia.
Wenhua ZhengFaculty of Health Sciences, University of Macau, Taipa, China.
Peter J LittleSchool of Pharmacy, The University of Queensland, Pharmacy Australia Centre of Excellence, Woolloongabba, QLD, Australia.
Narin OsmanSchool of Pharmacy, The University of Queensland, Pharmacy Australia Centre of Excellence, Woolloongabba, QLD, Australia.
The University of Queensland · AURMIT University · AUSun Yat-sen University · CNUniversity of Macau · MO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

G protein coupled receptor (GPCR) signalling covers three major mechanisms. GPCR agonist engagement allows for the G proteins to bind to the receptor leading to a classical downstream signalling cascade. The second mechanism is via the utilization of the β-arrestin signalling molecule and thirdly via transactivation dependent signalling. GPCRs can transactivate protein tyrosine kinase receptors (PTKR) to activate respective downstream signalling intermediates. In the past decade GPCR transactivation dependent signalling was expanded to show transactivation of serine/threonine kinase receptors (S/TKR). Kinase receptor transactivation enormously broadens the GPCR signalling paradigm. This work utilizes next generation RNA-sequencing to study the contribution of transactivation dependent signalling to total protease activated receptor (PAR)-1 signalling. Transactivation, assessed as gene expression, accounted for 50 percent of the total genes regulated by thrombin acting through PAR-1 in human coronary artery smooth muscle cells. GPCR transactivation of PTKRs is approximately equally important as the transactivation of the S/TKR with 209 and 177 genes regulated respectively, via either signalling pathway. This work shows that genome wide studies can provide powerful insights into GPCR mediated signalling pathways.

Indexed as

Sequence Analysis, RNASignal TransductionTranscriptional ActivationCoronary VesselsDown-RegulationGene Expression ProfilingHumansMuscle, Smooth, VascularProtein Serine-Threonine KinasesReceptor Protein-Tyrosine KinasesReceptors, G-Protein-CoupledUp-RegulationProtein Serine-Threonine KinasesReceptor Protein-Tyrosine KinasesReceptors, G-Protein-Coupled

Identifiers

PMID28719611
PMCPMC5515425
OpenAlexW2739235298

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.