Evidence map›Paper›PMID 28772122›Full record

ArticleNeuron2017

A C1-C2 Module in Munc13 Inhibits Calcium-Dependent Neurotransmitter Release.

Francesco Michelassi, Haowen Liu, Zhitao Hu, Jeremy S Dittman

Open access · bronzeAbstract read
In one paragraph

Article in Neuron, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

54 citing papers in PubMed, 86 citations in OpenAlex.

  1. Article
  2. Munc13 serves as a molecular filter for SNARE sorting and assembly in active zone condensates.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Article
  4. Single nucleotide variants inBiochemistry and biophysics reports · 2026
    Article
  5. Munc13-1 couples DAG and CaScience advances · 2026
    Article
  6. Article
  7. InhibitingBiomedicines · 2025
    Article
  8. Monoamine-induced diacylglycerol signaling rapidly accumulates Unc13 in nanoclusters for fast presynaptic potentiation.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  9. Article
  10. Article
  11. A specific negatively charged sequence confers intramolecular regulation on Munc13-1 function in synaptic exocytosis.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  12. Article
  13. Review
  14. Article
  15. Fully-primed slowly-recovering vesicles mediate presynaptic LTP at neocortical neurons.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  16. Roles for diacylglycerol in synaptic vesicle priming and release revealed by complete reconstitution of core protein machinery.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  17. Article
  18. Article
  19. Presynaptic Cytomatrix Proteins.Advances in neurobiology · 2023
    Article
  20. 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

4 authors at 3 institutions in 2 countries.

Francesco MichelassiDepartment of Biochemistry, Weill Cornell Medical College, 1300 York Avenue, New York, NY 10065, USA.
Haowen LiuQueensland Brain Institute, Clem Jones Centre for Ageing Dementia Research (CJCADR), University of Queensland, Brisbane, 4072 QLD, Australia.
Zhitao HuQueensland Brain Institute, Clem Jones Centre for Ageing Dementia Research (CJCADR), University of Queensland, Brisbane, 4072 QLD, Australia.
Jeremy S DittmanDepartment of Biochemistry, Weill Cornell Medical College, 1300 York Avenue, New York, NY 10065, USA. Electronic address: jed2019@med.cornell.edu.
Cornell University · USPark Centre for Mental Health · AUUniversity of Queensland · AU

Funding

Weill Cornell/Rockefeller/Sloan-Kettering MST ProgramT32GM007739 · NIGMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI HSU, KATHARINE C · 1985 to 2023
$51.1M
Analysis of synaptic protein dynamicsR01GM095674 · NIGMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI DITTMAN, JEREMY SAMUEL · 2011 to 2019
$3.2M
NIGMS NIH HHS R01 GM095674NIGMS NIH HHS T32 GM007739
6 · The paper itself

Abstract

Almost all known forms of fast chemical synaptic transmission require the synaptic hub protein Munc13. This essential protein has also been implicated in mediating several forms of use-dependent plasticity, but the mechanisms by which it controls vesicle fusion and plasticity are not well understood. Using the C. elegans Munc13 ortholog UNC-13, we show that deletion of the C2B domain, the most highly conserved domain of Munc13, enhances calcium-dependent exocytosis downstream of vesicle priming, revealing a novel autoinhibitory role for the C2B. Furthermore, C2B inhibition is relieved by calcium binding to C2B, while the neighboring C1 domain acts together with C2B to stabilize the autoinhibited state. Selective disruption of Munc13 autoinhibition profoundly impacts nervous system function in vivo. Thus, C1-C2B exerts a basal inhibition on Munc13 in the primed state, permitting calcium- and lipid-dependent control of C1-C2B to modulate synaptic strength.

Indexed as

Synaptic TransmissionAnimalsBiological TransportCaenorhabditis elegansCalciumCarrier ProteinsExocytosisMembrane FusionMembrane ProteinsNeurotransmitter AgentsSynaptic VesiclesCalciumCarrier ProteinsMembrane ProteinsNeurotransmitter Agentsphorbol ester binding proteinC1C2calciumC. elegansDAGfusionMunc13primingsynapseunc-13

Identifiers

PMID28772122
PMCPMC5569903
OpenAlexW2741499489

What OpenQuestion holds

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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.