Evidence map›Paper›PMID 18037927›Full record

ReviewBritish journal of pharmacology2008

Beta-arrestins and heterotrimeric G-proteins: collaborators and competitors in signal transduction.

K Defea

Abstract readReview
In one paragraph

Review in British journal of pharmacology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 1 pooled it
–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

67 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Endothelin-converting enzyme 2 regulates κ opioid receptor trafficking and function.The Journal of pharmacology and experimental therapeutics · 2025
    Article
  4. Article
  5. Review
  6. Regulation of CXCR4 function by S1PCell communication and signaling : CCS · 2025
    Article
  7. Dopamine, Immunity, and Disease.Pharmacological reviews · 2023
    Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Trypsin-Like Proteases and Their Role in Muco-Obstructive Lung Diseases.International journal of molecular sciences · 2021
    Review
  13. Phosphorylation barcode-dependent signal bias of the dopamine D1 receptor.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  14. Biased signaling by endogenous opioid peptides.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  15. Review
  16. Article
  17. Pancreatic islet inflammation: an emerging role for chemokines.Journal of molecular endocrinology · 2017
    Review
  18. Review
  19. Article
  20. Article

7 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

1 author.

K DefeaBiomedical Sciences Division, University of California, Riverside, 1620 Computer Statistics Bldg, Riverside, CA 92521, USA. kathryn.defea@ucr.edu

Funding

Molecular Scaffolds Direct MAPK Signaling SpecificityR01GM066151 · NIGMS · UNIVERSITY OF CALIFORNIA RIVERSIDE · PI DEFEA, KATHRYN ANNE · 2004 to 2009
$1.3M
NIGMS NIH HHS R01 GM066151NIGMS NIH HHS R01GM066151
6 · The paper itself

Abstract

G-protein-coupled receptors (GPCRs), also known as seven transmembrane receptors (7-TMRs), are the largest protein receptor superfamily in the body. These receptors and their ligands direct a diverse array of physiological responses, and hence have broad relevance to numerous diseases. As a result, they have generated considerable interest in the pharmaceutical industry as drug targets. Recently, GPCRs have been demonstrated to elicit signals through interaction with the scaffolding proteins, beta-arrestins-1 and 2, independent of heterotrimeric G-protein coupling. This review discusses several known G-protein-independent, beta-arrestin-dependent pathways and their potential physiological and pharmacological significance. The emergence of G-protein-independent signalling changes the way in which GPCR signalling is evaluated, from a cell biological to a pharmaceutical perspective and raises the possibility for the development of pathway specific therapeutics.

Indexed as

Actin Depolymerizing FactorsAnimalsArrestinsbeta-ArrestinsEnzyme ActivationGTP-Binding ProteinsHumansMitogen-Activated Protein KinasesNF-kappa BPhosphatidylinositol 3-KinasesSignal TransductionActin Depolymerizing FactorsArrestinsbeta-ArrestinsGTP-Binding ProteinsMitogen-Activated Protein KinasesNF-kappa BPhosphatidylinositol 3-Kinases

Identifiers

PMID18037927
PMCPMC2268080

What OpenQuestion holds

Textmetadata
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.