Evidence map›Paper›PMID 27071343›Full record

ReviewBiochemical pharmacology2016

The impact of RGS and other G-protein regulatory proteins on Gαi-mediated signaling in immunity.

John H Kehrl

Open access · greenAbstract readReview
In one paragraph

Review in Biochemical pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

37 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Gαi1/3 Is a Novel Regulatory Target for RANKL Signal Transduction and Osteoporosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Targeting GαBasic research in cardiology · 2024
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. 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

1 author at 1 institution in 1 country.

John H KehrlLaboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 2089, United States. Electronic address: jkehrl@niaid.nih.gov.
National Institutes of Health · US

Funding

Control Of G Protein Signaling: Role Of The RGSsZIAAI000738 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI KEHRL, JOHN H · 2009 to 2025
$15.9M
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
CONTROL OF G PROTEIN SIGNALING: ROLE OF THE RGSSZ01AI000738 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI KEHRL, JOHN H · 1996 to 2008
$3.9M
Intramural NIH HHS Z01 AI000738
6 · The paper itself

Abstract

Leukocyte chemoattractant receptors are members of the G-protein coupled receptor (GPCR) family. Signaling downstream of these receptors directs the localization, positioning and homeostatic trafficking of leukocytes; as well as their recruitment to, and their retention at, inflammatory sites. Ligand induced changes in the molecular conformation of chemoattractant receptors results in the engagement of heterotrimeric G-proteins, which promotes α subunits to undergo GTP/GDP exchange. This results in the functional release of βγ subunits from the heterotrimers, thereby activating downstream effector molecules, which initiate leukocyte polarization, gradient sensing, and directional migration. Pertussis toxin ADP ribosylates Gαi subunits and prevents chemoattractant receptors from triggering Gαi nucleotide exchange. The use of pertussis toxin revealed the essential importance of Gαi subunit nucleotide exchange for chemoattractant receptor signaling. More recent studies have identified a range of regulatory mechanisms that target these receptors and their associated heterotrimeric G-proteins, thereby helping to control the magnitude, kinetics, and duration of signaling. A failure in these regulatory pathways can lead to impaired receptor signaling and immunopathology. The analysis of mice with targeted deletions of Gαi isoforms as well as some of these G-protein regulatory proteins is providing insights into their roles in chemoattractant receptor signaling.

Indexed as

AnimalsChemotaxis, LeukocyteGTP-Binding Protein alpha Subunits, Gi-GoHumansImmune SystemPertussis ToxinReceptors, G-Protein-CoupledRGS ProteinsSignal TransductionGTP-Binding Protein alpha Subunits, Gi-GoPertussis ToxinReceptors, G-Protein-CoupledRGS ProteinsCell traffickingChemokine receptorsG-proteinRGS proteinsSphingosine 1-phosphate

Identifiers

PMID27071343
PMCPMC4993105
OpenAlexW2325313665

What Socratic 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 Socratic graph.