Evidence map›Paper›PMID 28035079›Full record

ReviewBiomolecules & therapeutics2017

Biased G Protein-Coupled Receptor Signaling: New Player in Modulating Physiology and Pathology.

Zuzana Bologna, Jian-Peng Teoh, Ahmed S Bayoumi, Yaoliang Tang, Il-Man Kim

Open access · greenAbstract readReview
In one paragraph

Review in Biomolecules & therapeutics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
7.5field-weighted citation impact, top 2% 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

48 citing papers in PubMed, 105 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. Identification of a β-arrestin-biased negative allosteric modulator for the βProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  7. State and Future Science of Opioids and Potential of Biased-ligand Technology in the Management of Acute Pain After Burn Injury.Journal of burn care & research : official publication of the American Burn Association · 2023
    Review
  8. Article
  9. Endogenous Derivatives of Linoleic Acid and their Stable Analogs Are Potential Pain Mediators.JID innovations : skin science from molecules to population health · 2023
    Article
  10. Pharmacognosy and Effects of Cannabinoids in the Vascular System.ACS pharmacology & translational science · 2022
    Review
  11. Lysyl oxidase promotes renal fibrosis via accelerating collagen cross-link driving by β-arrestin/ERK/STAT3 pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
    Article
  12. Review
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  17. Article
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  19. Review
  20. A computational model for GPCR-ligand interaction prediction.Journal of integrative bioinformatics · 2020
    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

5 authors at 1 institution in 1 country.

Zuzana BolognaVascular Biology Center, Medical College of Georgia, Augusta University, GA 30912, USA.
Jian-Peng TeohVascular Biology Center, Medical College of Georgia, Augusta University, GA 30912, USA.
Ahmed S BayoumiVascular Biology Center, Medical College of Georgia, Augusta University, GA 30912, USA.
Yaoliang TangVascular Biology Center, Medical College of Georgia, Augusta University, GA 30912, USA.
Il-Man KimVascular Biology Center, Medical College of Georgia, Augusta University, GA 30912, USA.
Augusta University · US

Funding

Beta-arrestin signaling and microRNA biogenesis in cardioprotectionR01HL124251 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI KIM, IL-MAN · 2014 to 2018
$1.9M
American Heart Association-American Stroke Association 14SDG18970040NHLBI NIH HHS R01 HL124251
6 · The paper itself

Abstract

G protein-coupled receptors (GPCRs) are a family of cell-surface proteins that play critical roles in regulating a variety of pathophysiological processes and thus are targeted by almost a third of currently available therapeutics. It was originally thought that GPCRs convert extracellular stimuli into intracellular signals through activating G proteins, whereas β-arrestins have important roles in internalization and desensitization of the receptor. Over the past decade, several novel functional aspects of β-arrestins in regulating GPCR signaling have been discovered. These previously unanticipated roles of β-arrestins to act as signal transducers and mediators of G protein-independent signaling have led to the concept of biased agonism. Biased GPCR ligands are able to engage with their target receptors in a manner that preferentially activates only G protein- or β-arrestin-mediated downstream signaling. This offers the potential for next generation drugs with high selectivity to therapeutically relevant GPCR signaling pathways. In this review, we provide a summary of the recent studies highlighting G protein- or β-arrestin-biased GPCR signaling and the effects of biased ligands on disease pathogenesis and regulation.

Indexed as

biased signalingG proteinG protein-coupled receptorβ-arrestin

Identifiers

PMID28035079
PMCPMC5207460
OpenAlexW2561886516

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.