Evidence map›Paper›PMID 24003153›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2013

Reprogramming of G protein-coupled receptor recycling and signaling by a kinase switch.

Rachel Vistein, Manojkumar A Puthenveedu

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

31 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
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  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Membrane Heterogeneity Controls Cellular Endocytic Trafficking.Frontiers in cell and developmental biology · 2020
    Review
  10. Article
  11. Article
  12. Spatial encoding of GPCR signaling in the nervous system.Current opinion in cell biology · 2019
    Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. A PTEN-Regulated Checkpoint Controls Surface Delivery of δ Opioid Receptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    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

2 authors at 1 institution in 1 country.

Rachel VisteinDepartment of Biological Sciences, Center for the Neural Basis of Cognition, Carnegie Mellon University, Pittsburgh, PA 15213.
Manojkumar A Puthenveedu
Center for the Neural Basis of Cognition · US

Funding

Multimodal Neuroimaging Training ProgramR90DA023420 · NIDA · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GIANAROS, PETER J · 2006 to 2015
$3.1M
Regulation of Clathrin-Coated Pits by the Mu-Opioid ReceptorR00DA024698 · NIDA · CARNEGIE-MELLON UNIVERSITY · PI PUTHENVEEDU, MANOJKUMAR A · 2009 to 2011
$735k
NIDA NIH HHS R00 DA024698NIDA NIH HHS R00-DA024698NIDA NIH HHS R90 DA023420NIDA NIH HHS T90-DA023420
6 · The paper itself

Abstract

The postendocytic recycling of signaling receptors is subject to multiple requirements. Why this is so, considering that many other proteins can recycle without apparent requirements, is a fundamental question. Here we show that cells can leverage these requirements to switch the recycling of the beta-2 adrenergic receptor (B2AR), a prototypic signaling receptor, between sequence-dependent and bulk recycling pathways, based on extracellular signals. This switch is determined by protein kinase A-mediated phosphorylation of B2AR on the cytoplasmic tail. The phosphorylation state of B2AR dictates its partitioning into spatially and functionally distinct endosomal microdomains mediating bulk and sequence-dependent recycling, and also regulates the rate of B2AR recycling and resensitization. Our results demonstrate that G protein-coupled receptor recycling is not always restricted to the sequence-dependent pathway, but may be reprogrammed as needed by physiological signals. Such flexible reprogramming might provide a versatile method for rapidly modulating cellular responses to extracellular signaling.

Indexed as

ProteolysisCyclic AMP-Dependent Protein KinasesEndosomesHEK293 CellsHumansMicroscopy, ConfocalModels, BiologicalPhosphorylationReceptors, Adrenergic, beta-2Signal TransductionCyclic AMP-Dependent Protein KinasesReceptors, Adrenergic, beta-2catecholamine receptorendosomal tubuleendosomesorting

Identifiers

PMID24003153
PMCPMC3780909
OpenAlexW2085004994

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.