Evidence map›Paper›PMID 11839771›Full record

ArticleThe Journal of cell biology2002

G protein-coupled receptor/arrestin3 modulation of the endocytic machinery.

Francesca Santini, Ibragim Gaidarov, James H Keen

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

42 citing papers in PubMed, 109 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. β-arrestin-dependent PI(4,5)PProceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  5. Review
  6. Spatial encoding of GPCR signaling in the nervous system.Current opinion in cell biology · 2019
    Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Trafficking of β-Adrenergic Receptors: Implications in Intracellular Receptor Signaling.Progress in molecular biology and translational science · 2015
    Review
  12. Nycthemeral variation in melatonin receptor expression in the lymphoid organs of a tropical seasonal breeder Funambulus pennanti.Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology · 2014
    Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Endocytosis and signalling: intertwining molecular networks.Nature reviews. Molecular cell biology · 2009
    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

3 authors at 1 institution in 1 country.

Francesca SantiniKimmel Cancer Institute and the Department of Microbiology and Immunology, Thomas Jefferson University, Philadelphia, PA 19107, USA.
Ibragim Gaidarov
James H Keen
Thomas Jefferson University · US

Funding

CLATHRIN AND MEMBRANE FUNCTIONR01GM028526 · NIGMS · THOMAS JEFFERSON UNIVERSITY · PI KEEN, JAMES H · 1985 to 2004
$1.2M
NIGMS NIH HHS GM-28526NIGMS NIH HHS R01 GM028526
6 · The paper itself

Abstract

Nonvisual arrestins (arr) modulate G protein-coupled receptor (GPCR) desensitization and internalization and bind to both clathrin (CL) and AP-2 components of the endocytic coated pit (CP). This raises the possibility that endocytosis of some GPCRs may be a consequence of arr-induced de novo CP formation. To directly test this hypothesis, we examined the behavior of green fluorescent protein (GFP)-arr3 in live cells expressing beta2-adrenergic receptors and fluorescent CL. After agonist stimulation, the diffuse GFP-arr3 signal rapidly became punctate and colocalized virtually completely with preexisting CP spots, demonstrating that activated complexes accumulate in previously formed CPs rather than nucleating new CP formation. After arr3 recruitment, CP appeared larger: electron microscopy analysis revealed an increase in both CP number and in the occurrence of clustered CPs. Mutant arr3 proteins with impaired binding to CL or AP-2 displayed reduced recruitment to CPs, but were still capable of inducing CP clustering. In contrast, though constitutively present in CPs, the COOH-terminal moiety of arr3, which contains CP binding sites but lacks receptor binding, did not induce CP clustering. Together, these results indicate that recruitment of functional arr3-GPCR complexes to CP is necessary to induce clustering. Latrunculin B or 16 degrees C blocked CP rearrangements without affecting arr3 recruitment to CP. These results and earlier studies suggest that discrete CP zones exist on cell surfaces, each capable of supporting adjacent CPs, and that the cortical actin membrane skeleton is intimately involved with both the maintenance of existing CPs and the generation of new structures.

Indexed as

Adrenergic beta-AgonistsAnimalsArrestinsBridged Bicyclo Compounds, HeterocyclicCell LineChlorocebus aethiopsCoated Pits, Cell-MembraneCOS CellsEndocytosisGTP-Binding ProteinsHumansImage Processing, Computer-AssistedIsoproterenolReceptor, Muscarinic M1Receptors, Adrenergic, beta-2Receptors, Cell SurfaceAdrenergic beta-Agonistsarrestin3ArrestinsBridged Bicyclo Compounds, HeterocyclicGTP-Binding ProteinsIsoproterenollatrunculin BReceptor, Muscarinic M1Receptors, Adrenergic, beta-2Receptors, Cell SurfaceReceptors, MuscarinicRecombinant Fusion ProteinsThiazolesThiazolidines

Identifiers

PMID11839771
PMCPMC2174075
OpenAlexW2103481821

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.