Evidence map›Paper›PMID 16793874›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006

Structural determinants of synaptobrevin 2 function in synaptic vesicle fusion.

Ferenc Deák, Ok-Ho Shin, Ege T Kavalali, Thomas C Südhof

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed
4.1field-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

84 citing papers in PubMed, 146 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Genetic disorders of neurotransmitter release machinery.Frontiers in synaptic neuroscience · 2023
    Review
  5. The function of VAMP2 in mediating membrane fusion: An overview.Frontiers in molecular neuroscience · 2022
    Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Age-Related Cognitive Impairment: Role of Reduced Synaptobrevin-2 Levels in Deficits of Memory and Synaptic Plasticity.The journals of gerontology. Series A, Biological sciences and medical sciences · 2020
    Article
  12. Article
  13. Article
  14. Ablation of All Synaptobrevin vSNAREs Blocks Evoked But Not Spontaneous Neurotransmitter Release at Neuromuscular Synapses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Mechanism of neurotransmitter release coming into focus.Protein science : a publication of the Protein Society · 2018
    Review
  20. Article

24 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Ferenc DeákCenter for Basic Neuroscience, The University of Texas Southwestern Medical Center, Dallas, Texas 75390-9111, USA.
Ok-Ho Shin
Ege T Kavalali
Thomas C Südhof
The University of Texas Southwestern Medical Center · USHoward Hughes Medical Institute · US

Funding

Role of SNARE Interactions in Central Synapse FunctionR01MH066198 · NIMH · VANDERBILT UNIVERSITY · PI KAVALALI, EGE T · 2004 to 2023
$7.9M
NIMH NIH HHS MH066198
6 · The paper itself

Abstract

Deletion of synaptobrevin/vesicle-associated membrane protein, the major synaptic vesicle soluble N-ethylmaleimide-sensitive factor attachment protein receptor (R-SNARE), severely decreases but does not abolish spontaneous and evoked synaptic vesicle exocytosis. We now show that the closely related R-SNARE protein cellubrevin rescues synaptic transmission in synaptobrevin-deficient neurons but that deletion of both cellubrevin and synaptobrevin does not cause a more severe decrease in exocytosis than deletion of synaptobrevin alone. We then examined the structural requirements for synaptobrevin to function in exocytosis. We found that substituting glutamine for arginine in the zero-layer of the SNARE motif did not significantly impair synaptobrevin-dependent exocytosis, whereas insertion of 12 or 24 residues between the SNARE motif and transmembrane region abolished the ability of synaptobrevin to mediate Ca2+-evoked exocytosis. Surprisingly, however, synaptobrevin with the 12-residue but not the 24-residue insertion restored spontaneous release in synaptobrevin-deficient neurons. Our data suggest that synaptobrevin mediates Ca2+-triggered exocytosis by tight coupling of the SNARE motif to the transmembrane region and hence forcing the membranes into close proximity for fusion. Furthermore, the fusion reactions underlying evoked and spontaneous release differ mechanistically.

Indexed as

AnimalsAnimals, NewbornCells, CulturedCloning, MolecularElectric StimulationExcitatory Postsynaptic PotentialsHippocampusImmunoprecipitationInfectionsMembrane FusionMembrane PotentialsMiceMice, KnockoutMutationNeuronsSNARE ProteinsSNARE ProteinsSyntaxin 1Vesicle-Associated Membrane Protein 2Vesicle-Associated Membrane Protein 3

Identifiers

PMID16793874
PMCPMC6673840
OpenAlexW1988488160

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.