Evidence map›Paper›PMID 21680031›Full record

ReviewTrends in pharmacological sciences2011

β-Arrestin-mediated receptor trafficking and signal transduction.

Sudha K Shenoy, Robert J Lefkowitz

Abstract readReview
In one paragraph

Review in Trends in pharmacological sciences, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 371 papers.

0numbers the graph read from it
0cells of the map it votes in
371citing papers in PubMed
24.1field-weighted citation impact, top 1% 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

371 citing papers in PubMed, 695 citations in OpenAlex.

  1. Trial
  2. Beta-Arrestin-2 Binds to Nucleolar Organizing Regions With P2X7 Receptor Stimulation and During Cell Division.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  3. Article
  4. Article
  5. Review
  6. Dopamine supersensitivity psychosis: a critical evaluation of diagnostic validators.Journal of neural transmission (Vienna, Austria : 1996) · 2026
    Review
  7. Review
  8. Beta arrestin 1 is a key regulator of pulmonary vascular tone.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  9. Article
  10. Histamine HPharmaceuticals (Basel, Switzerland) · 2026
    Article
  11. Review
  12. Article
  13. Structural Basis of GPCR-Biased Modulation.Handbook of experimental pharmacology · 2026
    Review
  14. Review
  15. Article
  16. Article
  17. Platelet Membrane Receptors and Signalling Pathways.Handbook of experimental pharmacology · 2026
    Review
  18. Review
  19. Future Directions in GPCR Biased Signaling and Ligand Pharmacology.Handbook of experimental pharmacology · 2026
    Review
  20. Review

311 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

2 authors at 2 institutions in 1 country.

Sudha K ShenoyDepartment of Medicine, Duke University Medical Center, Box 3821, Durham, NC 27710, USA. sudha@receptor-biol.duke.edu
Robert J Lefkowitz
Duke University · USDuke University Hospital · US

Funding

Molecular Regulation of Cardiovascular 7 TM ReceptorsR01HL016037 · NHLBI · DUKE UNIVERSITY · PI ROBERT J LEFKOWITZ · 1985 to 2026
$14.5M
B-Arrestins and G Protein-Coupled Receptor Kinases in Cardiovascular FunctionR01HL070631 · NHLBI · DUKE UNIVERSITY · PI LEFKOWITZ, ROBERT J · 2002 to 2011
$3.5M
E3 Ligases and Deubiquitinases in GPCR Down RegulationR01HL080525 · NHLBI · DUKE UNIVERSITY · PI SHENOY, SUDHA K · 2005 to 2014
$3.3M
NHLBI NIH HHS R01 HL016037NHLBI NIH HHS R01 HL070631NHLBI NIH HHS R01 HL080525
6 · The paper itself

Abstract

β-Arrestins function as endocytic adaptors and mediate trafficking of a variety of cell-surface receptors, including seven-transmembrane receptors (7TMRs). In the case of 7TMRs, β-arrestins carry out these tasks while simultaneously inhibiting upstream G-protein-dependent signaling and promoting alternate downstream signaling pathways. The mechanisms by which β-arrestins interact with a continuously expanding ensemble of protein partners and perform their multiple functions including trafficking and signaling are currently being uncovered. Molecular changes at the level of protein conformation as well as post-translational modifications of β-arrestins probably form the basis for their dynamic interactions during receptor trafficking and signaling. It is becoming increasingly evident that β-arrestins, originally discovered as 7TMR adaptor proteins, indeed have much broader and more versatile roles in maintaining cellular homeostasis. In this review paper, we assess the traditional and novel functions of β-arrestins and discuss the molecular attributes that might facilitate multiple interactions in regulating cell signaling and receptor trafficking.

Indexed as

Signal TransductionAnimalsArrestinsbeta-ArrestinsHumansProtein ConformationProtein Processing, Post-TranslationalProtein TransportReceptors, G-Protein-CoupledArrestinsbeta-ArrestinsReceptors, G-Protein-Coupledseven-transmembrane G-protein-coupled receptor

Identifiers

PMID21680031
PMCPMC3159699
OpenAlexW2165488941

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.