Evidence map›Paper›PMID 24583286›Full record

ReviewCellular signalling2014

Implications of non-canonical G-protein signaling for the immune system.

Cédric Boularan, John H Kehrl

Open access · greenAbstract readReview
In one paragraph

Review in Cellular signalling, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

18 citing papers in PubMed, 27 citations in OpenAlex.

  1. Virulence · 2026
    Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Regulation of Chemokine Signal Integration by Activator of G-Protein Signaling 4 (AGS4).The Journal of pharmacology and experimental therapeutics · 2017
    Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. CXCR4: a virus's best friend?Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2014
    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

2 authors at 2 institutions in 1 country.

Cédric BoularanB-cell Molecular Immunology Section, Laboratory of Immunoregulation, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, United States.
John H KehrlB-cell Molecular Immunology Section, Laboratory of Immunoregulation, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, United States. Electronic address: jkehrl@niaid.nih.gov.
National Institute of Allergy and Infectious Diseases · USNational Institutes of Health · US

Funding

Signal Transduction In B Lymphocytes: Identification Of Key Signaling MoleculesZIAAI000739 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI KEHRL, JOHN H · 2009 to 2025
$17.8M
Analysis of the Functional Roles of a Novel G-alpha Nucleotide CycleZIAAI000961 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI KEHRL, JOHN H · 2009 to 2018
$4.4M
SIGNAL TRANSDUCTION IN B LYMPHOCYTES: INDENTIFICATION OF KEY SIGNALING MOLECULEZ01AI000739 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI KEHRL, JOHN H · 1996 to 2008
$1.5M
Intramural NIH HHS Z01 AI000739
6 · The paper itself

Abstract

Heterotrimeric guanine nucleotide-binding proteins (G proteins), which consist of three subunits α, β, and γ, function as molecular switches to control downstream effector molecules activated by G protein-coupled receptors (GPCRs). The GTP/GDP binding status of Gα transmits information about the ligand binding state of the GPCR to intended signal transduction pathways. In immune cells heterotrimeric G proteins impact signal transduction pathways that directly, or indirectly, regulate cell migration, activation, survival, proliferation, and differentiation. The cells of the innate and adaptive immune system abundantly express chemoattractant receptors and lesser amounts of many other types of GPCRs. But heterotrimeric G-proteins not only function in classical GPCR signaling, but also in non-canonical signaling. In these pathways the guanine exchange factor (GEF) exerted by a GPCR in the canonical pathway is replaced or supplemented by another protein such as Ric-8A. In addition, other proteins such as AGS3-6 can compete with Gβγ for binding to GDP bound Gα. This competition can promote Gβγ signaling by freeing Gβγ from rapidly rebinding GDP bound Gα. The proteins that participate in these non-canonical signaling pathways will be briefly described and their role, or potential one, in cells of the immune system will be highlighted.

Indexed as

AnimalsGene ExpressionHeterotrimeric GTP-Binding ProteinsHumansImmune SystemImmunity, CellularImmunity, InnateReceptor Protein-Tyrosine KinasesReceptors, G-Protein-CoupledSignal TransductionHeterotrimeric GTP-Binding ProteinsReceptor Protein-Tyrosine KinasesReceptors, G-Protein-CoupledG-protein signalingImmune systemNon-canonicalRic-8A

Identifiers

PMID24583286
PMCPMC4116820
OpenAlexW1978651209

What OpenQuestion holds

Textmetadata
LicenceTDM
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.