Evidence map›Paper›PMID 28328745›Full record

ReviewJournal of cardiovascular pharmacology2017

G Protein-Coupled Receptor Signaling Through β-Arrestin-Dependent Mechanisms.

Pierre-Yves Jean-Charles, Suneet Kaur, Sudha K Shenoy

Open access · greenAbstract readReview
In one paragraph

Review in Journal of cardiovascular pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 153 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
153citing papers in PubMed, 1 pooled it
6.2field-weighted citation impact, top 3% 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

153 citing papers in PubMed, 1 synthesis or guideline pooled it, 266 citations in OpenAlex.

  1. The Signaling and Pharmacology of the Dopamine D1 Receptor.Frontiers in cellular neuroscience · 2021
    Pooled it
  2. Article
  3. The CX3CL1-CX3CR1 axis in HIV-associated inflammation and cardiometabolic disease.American journal of physiology. Regulatory, integrative and comparative physiology · 2026
    Review
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  19. β-Adrenergic Receptors: Not Always Outside-In.Physiology (Bethesda, Md.) · 2026
    Review
  20. Review

93 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 2 countries.

Pierre-Yves Jean-CharlesDepartments of *Medicine (Cardiology); and †Cell Biology, Duke University Medical Center, Durham, NC.
Suneet Kaur
Sudha K Shenoy
Institute of Cardiology · PLDuke Medical Center · US

Funding

Renal Genomics CoreP30DK096493 · NIDDK · DUKE UNIVERSITY · PI PATEL, UPTAL D · 2012 to 2016
$5.9M
E3 Ligases and Deubiquitinases in GPCR Down RegulationR01HL080525 · NHLBI · DUKE UNIVERSITY · PI SHENOY, SUDHA K · 2005 to 2014
$3.3M
Regulation of B-arrestin2's pro-atherogenic activity by the deubiquitinase USP20R01HL118369 · NHLBI · DUKE UNIVERSITY · PI FREEDMAN, NEIL J., SHENOY, SUDHA K · 2014 to 2017
$2.1M
NHLBI NIH HHS R01 HL080525NHLBI NIH HHS R01 HL118369NIDDK NIH HHS P30 DK096493
6 · The paper itself

Abstract

β-arrestin1 (or arrestin2) and β-arrestin2 (or arrestin3) are ubiquitously expressed cytosolic adaptor proteins that were originally discovered for their inhibitory role in G protein-coupled receptor (GPCR) signaling through heterotrimeric G proteins. However, further biochemical characterization revealed that β-arrestins do not just "block" the activated GPCRs, but trigger endocytosis and kinase activation leading to specific signaling pathways that can be localized on endosomes. The signaling pathways initiated by β-arrestins were also found to be independent of G protein activation by GPCRs. The discovery of ligands that blocked G protein activation but promoted β-arrestin binding, or vice-versa, suggested the exciting possibility of selectively activating intracellular signaling pathways. In addition, it is becoming increasingly evident that β-arrestin-dependent signaling is extremely diverse and provokes distinct cellular responses through different GPCRs even when the same effector kinase is involved. In this review, we summarize various signaling pathways mediated by β-arrestins and highlight the physiologic effects of β-arrestin-dependent signaling.

Indexed as

Animalsbeta-ArrestinsEndocytosisHumansReceptors, G-Protein-CoupledSignal Transductionbeta-ArrestinsReceptors, G-Protein-Coupled

Identifiers

PMID28328745
PMCPMC5591062
OpenAlexW2601465249

What OpenQuestion holds

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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.