Evidence map›Paper›PMID 24260568›Full record

ArticlePloS one2013

PKC and PKA regulate AChR dynamics at the neuromuscular junction of living mice.

Isabel Martinez-Pena y Valenzuela, Marcelo Pires-Oliveira, Mohammed Akaaboune

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
0.7field-weighted citation impact, top 29% 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

23 citing papers in PubMed, 34 citations in OpenAlex.

  1. Junctions in Jeopardy: the neuromuscular junction is a selective pathological target in Charcot-Marie-Tooth disease.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
    Review
  2. Article
  3. Article
  4. Aberrant evoked calcium signaling and nAChR cluster morphology in aFrontiers in cell and developmental biology · 2024
    Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Cardiac troponin T and fast skeletal muscle denervation in ageing.Journal of cachexia, sarcopenia and muscle · 2017
    Article
  19. Article
  20. Sympathetic innervation controls homeostasis of neuromuscular junctions in health and disease.Proceedings of the National Academy of Sciences of the United States of America · 2016
    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

3 authors at 2 institutions in 1 country.

Isabel Martinez-Pena y ValenzuelaDepartment of Molecular, Cellular and Developmental Biology, University of Michigan, Ann Arbor, Michigan, United States of America.
Marcelo Pires-Oliveira
Mohammed Akaaboune
Michigan United · USUniversity of Michigan–Ann Arbor · US

Funding

The Dynamics of Synaptic Component at the Neuromuscular Junction of Living AnimalR01NS047332 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI AKAABOUNE, MOHAMMED · 2003 to 2013
$2.7M
NINDS NIH HHS NS-047332NINDS NIH HHS R01 NS047332
6 · The paper itself

Abstract

The steady state of the acetylcholine receptor (AChR) density at the neuromuscular junction (NMJ) is critical for efficient and reliable synaptic transmission. However, little is known about signaling molecules involved in regulating the equilibrium between the removal and insertion of AChRs that establishes a stable postsynaptic receptor density over time. In this work, we tested the effect of activities of two serine/threonine kinases, PKC and PKA, on the removal rate of AChRs from and the re-insertion rate of internalized recycled AChRs into synaptic sites of innervated and denervated NMJs of living mice. Using an in vivo time-lapse imaging approach and various pharmacological agents, we showed that PKC and PKA activities have antagonistic effects on the removal and recycling of AChRs. Inhibition of PKC activity or activation of PKA largely prevents the removal of pre-existing AChRs and promotes the recycling of internalized AChRs into the postsynaptic membrane. In contrast, stimulation of PKC or inactivation of PKA significantly accelerates the removal of postsynaptic AChRs and depresses AChR recycling. These results indicate that a balance between PKA and PKC activities may be critical for the maintenance of the postsynaptic receptor density.

Indexed as

Synaptic Transmission8-Bromo Cyclic Adenosine MonophosphateAnimalsCyclic AMP-Dependent Protein KinasesEnzyme ActivatorsFemaleIsoquinolinesMiceMuscle DenervationNaphthalenesNeuromuscular JunctionPost-Synaptic DensityProtein Kinase CProtein Kinase InhibitorsProtein TransportReceptors, Cholinergic8-Bromo Cyclic Adenosine Monophosphatecalphostin CCyclic AMP-Dependent Protein KinasesEnzyme ActivatorsIsoquinolinesN-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamideNaphthalenesProtein Kinase CProtein Kinase InhibitorsReceptors, CholinergicSulfonamidesTetradecanoylphorbol Acetate

Identifiers

PMID24260568
PMCPMC3829966
OpenAlexW2023812792

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.