Evidence map›Paper›PMID 33600853›Full record

ReviewPharmacology & therapeutics2021

RGS proteins, GRKs, and beta-arrestins modulate G protein-mediated signaling pathways in asthma.

Nathalie Fuentes, Morgan McCullough, Reynold A Panettieri, Kirk M Druey

Open access · greenAbstract readReview
In one paragraph

Review in Pharmacology & therapeutics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Genetic variants of accessory proteins and G proteins in human genetic disease.Critical reviews in clinical laboratory sciences · 2025
    Review
  5. Powerful mapping ofmedRxiv : the preprint server for health sciences · 2024
    Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. 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

4 authors at 3 institutions in 1 country.

Nathalie FuentesLung and Vascular Inflammation Section, Laboratory of Allergic Diseases, NIAID/NIH, Bethesda, MD, United States of America.
Morgan McCulloughLung and Vascular Inflammation Section, Laboratory of Allergic Diseases, NIAID/NIH, Bethesda, MD, United States of America.
Reynold A PanettieriRutgers Institute for Translational Medicine and Science, Child Health Institute of New Jersey, Rutgers University School of Medicine, New Brunswick, NJ, United States of America.
Kirk M DrueyLung and Vascular Inflammation Section, Laboratory of Allergic Diseases, NIAID/NIH, Bethesda, MD, United States of America. Electronic address: kdruey@niaid.nih.gov.
National Institutes of Health · USNational Institute of Allergy and Infectious Diseases · USRutgers, The State University of New Jersey · US

Funding

Translational Research Support CoreP30ES005022 · NIEHS · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI BRIAN T BUCKLEY · 1988 to 2026
$47.4M
New Jersey Alliance for Clinical Translational Science: NJ ACTSUL1TR003017 · NCATS · RUTGERS BIOMEDICAL/HEALTH SCIENCES-RBHS · PI PANETTIERI, REYNOLD ALEXANDER · 2019 to 2023
$28.9M
Project 4 - OGR1- and TSPO- dependent mechanisms mediated by benzodiazepines affecting ASM contractionP01HL114471 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI LIGGETT, STEPHEN B · 2013 to 2023
$23.9M
Expanding Translational Research in ArkansasUL1TR003107 · NCATS · UNIV OF ARKANSAS FOR MED SCIS · PI JAMES, LAURA P · 2019 to 2023
$21.6M
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
Intramural NIH HHS Z01 AI000746NCATS NIH HHS UL1 TR003017NCATS NIH HHS UL1 TR003107NHLBI NIH HHS P01 HL114471NIEHS NIH HHS P30 ES005022
6 · The paper itself

Abstract

Asthma is a highly prevalent disorder characterized by chronic lung inflammation and reversible airways obstruction. Pathophysiological features of asthma include episodic and reversible airway narrowing due to increased bronchial smooth muscle shortening in response to external and host-derived mediators, excessive mucus secretion into the airway lumen, and airway remodeling. The aberrant airway smooth muscle (ASM) phenotype observed in asthma manifests as increased sensitivity to contractile mediators (EC

Indexed as

AsthmaGTP-Binding ProteinsReceptors, G-Protein-CoupledSignal Transductionbeta-ArrestinsG-Protein-Coupled Receptor KinasesHumansRGS Proteinsbeta-ArrestinsG-Protein-Coupled Receptor KinasesGTP-Binding ProteinsReceptors, G-Protein-CoupledRGS ProteinsAirway smooth muscleAsthmaGPCRRemodelingSignal transduction

Identifiers

PMID33600853
PMCPMC8192426
OpenAlexW3130284932

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.