Evidence map›Paper›PMID 18810336›Full record

ReviewImmunologic research2009

Regulation of G-protein-coupled signaling pathways in allergic inflammation.

Kirk M Druey

Open access · greenAbstract readReview
In one paragraph

Review in Immunologic research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.4field-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

23 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Article
  3. Can GPCRs Be Targeted to Control Inflammation in Asthma?Advances in experimental medicine and biology · 2021
    Article
  4. GαExperimental & molecular medicine · 2020
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Role of regulator of G protein signaling proteins in bone.Frontiers in bioscience (Landmark edition) · 2014
    Review
  14. RGS3 controls T lymphocyte migration in a model of Th2-mediated airway inflammation.American journal of physiology. Lung cellular and molecular physiology · 2013
    Article
  15. A finer tuning of G-protein signaling through regulated control of RGS proteins.American journal of physiology. Heart and circulatory physiology · 2012
    Review
  16. Article
  17. Article
  18. Review
  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.

Kirk M DrueyMolecular Signal Transduction Section, Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Disease, National Institutes of Health, 10 Center Drive Room 11N242, Bethesda, MD 20892, USA, kdruey@niaid.nih.gov
National Institutes of Health · US

Funding

Regulation of Normal and Asthmatic Lung Function by G-Protein-Coupled ReceptorsZIAAI000939 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI DRUEY, KIRK M · 2009 to 2025
$7.3M
Heterotrimeric G Protein Signaling In Allergic InflammationZIAAI000746 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI DRUEY, KIRK M · 2009 to 2025
$4.6M
HETEROTRIMERIC G PROTEIN SIGNALING IN ALLERGIC INFLAMMATIONZ01AI000746 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI DRUEY, KIRK M · 1998 to 2008
$1.1M
Regulation of Normal and Asthmatic Lung Function by G-Protein-Coupled ReceptorsZ01AI000939 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI DRUEY, KIRK M · 2004 to 2008
$832k
G-Protein-Coupled Signal Transduction in Urticaria and AnaphylaxisZ01AI000972 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI DRUEY, KIRK M · 2006 to 2008
$153k
G-Protein-Coupled Signal Transduction in Allergy and AnaphylaxisZIAAI000972 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI DRUEY, KIRK M · 2009 to 2009
$71k
Intramural NIH HHS Z01 AI000746Intramural NIH HHS Z01 AI000939Intramural NIH HHS Z01 AI000972Intramural NIH HHS Z99 AI999999
6 · The paper itself

Abstract

Allergic diseases such as asthma are elicited by maladaptive activation of immune cells such as mast cells and lymphocytes by otherwise innocuous allergens. The numerous mediators secreted by such cells promote both acute inflammation and, in many instances, chronic tissue remodeling. Most of these compounds exert their effects on end-organ targets such as epithelial and endothelial cells and airway smooth muscle by activating G-protein-coupled receptors (GPCRs), which are by far the most abundant type of cell surface receptor. Since GPCRs are also the most common target of allergy therapeutics, a better understanding of their intracellular signaling mechanisms is vital to improve the efficacy of such drugs or to develop new targets. In this review, we focus on some of the new regulatory elements that control the duration and amplitude of GPCR signal transduction pathways in immune effector cells and end-organ structural cells affected by allergic inflammation.

Indexed as

AnimalsB-LymphocytesCell MovementGTP-Binding ProteinsHumansHypersensitivityInflammationMast CellsReceptors, G-Protein-CoupledRGS ProteinsSignal TransductionT-LymphocytesGTP-Binding ProteinsReceptors, G-Protein-CoupledRGS Proteins

Identifiers

PMID18810336
PMCPMC2687145
OpenAlexW1980897262

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.