Evidence map›Paper›PMID 24520164›Full record

ArticleeLife2014

Munc18-1 is a dynamically regulated PKC target during short-term enhancement of transmitter release.

Ozgür Genc, Olexiy Kochubey, Ruud F Toonen, Matthijs Verhage, Ralf Schneggenburger

Open access · goldAbstract read
In one paragraph

Article in eLife, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

50 citing papers in PubMed, 71 citations in OpenAlex.

  1. Munc13-1 couples DAG and CaScience advances · 2026
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  5. Energetics, kinetics, and pathways of SNARE assembly in membrane fusion.Critical reviews in biochemistry and molecular biology · 2022
    Review
  6. Article
  7. Review
  8. Presynaptic Short-Term Plasticity Persists in the Absence of PKC Phosphorylation of Munc18-1.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  9. Chaperoning SNARE Folding and Assembly.Annual review of biochemistry · 2021
    Review
  10. Environmental Enrichment Enhances CaInternational journal of molecular sciences · 2021
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Diverse exocytic pathways for mast cell mediators.Biochemical Society transactions · 2018
    Review
  17. Article
  18. PKC-dependent phosphorylation of Munc18a at Ser313 in activated RBL-2H3 cells.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2018
    Article
  19. Article
  20. 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

5 authors at 3 institutions in 2 countries.

Ozgür GencLaboratory of Synaptic Mechanisms, Brain Mind Institute, School of Life Science, École Polytechnique Fédérale de Lausanne (EPFL), Lausanne, Switzerland.
Olexiy Kochubey
Ruud F Toonen
Matthijs Verhage
Ralf Schneggenburger
École Polytechnique Fédérale de Lausanne · CHAmsterdam Neuroscience · NLAmsterdam UMC Location VUmc · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transmitter release at synapses is regulated by preceding neuronal activity, which can give rise to short-term enhancement of release like post-tetanic potentiation (PTP). Diacylglycerol (DAG) and Protein-kinase C (PKC) signaling in the nerve terminal have been widely implicated in the short-term modulation of transmitter release, but the target protein of PKC phosphorylation during short-term enhancement has remained unknown. Here, we use a gene-replacement strategy at the calyx of Held, a large CNS model synapse that expresses robust PTP, to study the molecular mechanisms of PTP. We find that two PKC phosphorylation sites of Munc18-1 are critically important for PTP, which identifies the presynaptic target protein for the action of PKC during PTP. Pharmacological experiments show that a phosphatase normally limits the duration of PTP, and that PTP is initiated by the action of a 'conventional' PKC isoform. Thus, a dynamic PKC phosphorylation/de-phosphorylation cycle of Munc18-1 drives short-term enhancement of transmitter release during PTP. DOI: http://dx.doi.org/10.7554/eLife.01715.001.

Indexed as

AnimalsMiceMunc18 ProteinsNeurotransmitter AgentsProtein Kinase CSynapsesMunc18 ProteinsNeurotransmitter AgentsProtein Kinase CStxbp1 protein, mousecalyx of Heldprotein kinase Cprotein phosphatasesynaptic plasticitysynaptic transmissiontransmitter release

Identifiers

PMID24520164
PMCPMC3919271
OpenAlexW1986641384

What OpenQuestion holds

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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.