Evidence map›Paper›PMID 38906769›Full record

ReviewTrends in pharmacological sciences2024

GPCR-dependent and -independent arrestin signaling.

Vsevolod V Gurevich, Eugenia V Gurevich

Abstract readReview
In one paragraph

Review in Trends in pharmacological sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact
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

16 citing papers in PubMed.

  1. Article
  2. Article
  3. Intrinsic conformational equilibria position arrestin-2 for activation.Protein science : a publication of the Protein Society · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Intrinsic conformational equilibria position arrestin-2 for activation.bioRxiv : the preprint server for biology · 2025
    Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Arrestins as Possible Drug Targets.Biomolecules & therapeutics · 2025
    Review
  13. Review
  14. Review
  15. Article
  16. Review
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

2 authors.

Vsevolod V GurevichDepartment of Pharmacology, Vanderbilt University, Nashville, TN 27232, USA. Electronic address: vsevolod.gurevich@vanderbilt.edu.
Eugenia V GurevichDepartment of Pharmacology, Vanderbilt University, Nashville, TN 27232, USA.

Funding

STRUCTURE/FUNCTION STUDIES OF VISUAL ARRESTINR01EY011500 · NEI · VANDERBILT UNIVERSITY · PI T M Iverson · 1997 to 2026
$12.3M
Targeted Engineering of Designer Arrestins to Regulate Cell SignalingR35GM122491 · NIGMS · VANDERBILT UNIVERSITY · PI GUREVICH, VSEVOLOD V. · 2017 to 2021
$2.6M
NEI NIH HHS R01 EY011500NIGMS NIH HHS R35 GM122491
6 · The paper itself

Abstract

Biological activity of free arrestins is often overlooked. Based on available data, we compare arrestin-mediated signaling that requires and does not require binding to G-protein-coupled receptors (GPCRs). Receptor-bound arrestins activate ERK1/2, Src, and focal adhesion kinase (FAK). Yet, arrestin-3 regulation of Src family member Fgr does not appear to involve receptors. Free arrestin-3 facilitates the activation of JNK family kinases, preferentially binds E3 ubiquitin ligases Mdm2 and parkin, and facilitates parkin-dependent mitophagy. The binding of arrestins to microtubules and calmodulin and their function in focal adhesion disassembly and apoptosis also do not involve receptors. Biased GPCR ligands and the phosphorylation barcode can only affect receptor-dependent arrestin signaling. Thus, elucidation of receptor dependence or independence of arrestin functions has important scientific and therapeutic implications.

Indexed as

Receptors, G-Protein-CoupledSignal TransductionAnimalsArrestinsHumansArrestinsReceptors, G-Protein-Coupledarrestinbiased signalingGPCRphosphorylation barcode

Identifiers

PMID38906769
PMCPMC11227395

What OpenQuestion holds

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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.