Evidence map›Paper›PMID 32515733›Full record

ArticleeLife2020

Acute disruption of the synaptic vesicle membrane protein synaptotagmin 1 using knockoff in mouse hippocampal neurons.

Jason D Vevea, Edwin R Chapman

Abstract read
In one paragraph

Article in eLife, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
–field-weighted citation impact
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

29 citing papers in PubMed.

  1. Article
  2. Humanized extracellular vesicles for efficient RNA delivery.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Article
  4. Humanized Extracellular Vesicles for Efficient RNA Delivery.bioRxiv : the preprint server for biology · 2025
    Article
  5. Article
  6. Optimizing multifunctional fluorescent ligands for intracellular labeling.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  7. Article
  8. Fiber-basedNeurophotonics · 2024
    Article
  9. Article
  10. Phospholipids Differentially Regulate CaACS chemical biology · 2024
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. The SphK1/S1P Axis Regulates Synaptic Vesicle Endocytosis via TRPC5 Channels.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  16. Mitofusin 2 Sustains the Axonal Mitochondrial Network to Support Presynaptic CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  17. Synaptotagmin 9 Modulates Spontaneous Neurotransmitter Release in Striatal Neurons by Regulating Substance P Secretion.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  18. Article
  19. Polybasic Patches in Both C2 Domains of Synaptotagmin-1 Are Required for Evoked Neurotransmitter Release.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    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

2 authors.

Jason D VeveaDepartment of Neuroscience, University of Wisconsin-Madison, Madison, United States.ORCID 0000-0002-3068-973X
Edwin R ChapmanDepartment of Neuroscience, University of Wisconsin-Madison, Madison, United States.ORCID 0000-0001-9787-8140

Funding

Synaptotagmin C2B Domain as a Ca2+ Sensing ModuleR01MH061876 · NIMH · UNIVERSITY OF WISCONSIN-MADISON · PI Edwin R Chapman · 2002 to 2026
$7.7M
Structure and dynamics of exocytotic fusion poresR35NS097362 · NINDS · UNIVERSITY OF WISCONSIN-MADISON · PI CHAPMAN, EDWIN R · 2017 to 2024
$4.6M
Mechanisms regulating mitochondrial polarity in neurons: regional distribution and specializationF32NS098604 · NINDS · UNIVERSITY OF WISCONSIN-MADISON · PI VEVEA, JASON DANIEL · 2017 to 2019
$179k
NIH HHS MH061876NIH HHS NS097362NIH HHS NS098604NIMH NIH HHS R01 MH061876NINDS NIH HHS F32 NS098604NINDS NIH HHS R35 NS097362
6 · The paper itself

Abstract

The success of comparative cell biology for determining protein function relies on quality disruption techniques. Long-lived proteins, in postmitotic cells, are particularly difficult to eliminate. Moreover, cellular processes are notoriously adaptive; for example, neuronal synapses exhibit a high degree of plasticity. Ideally, protein disruption techniques should be both rapid and complete. Here, we describe knockoff, a generalizable method for the druggable control of membrane protein stability. We developed knockoff for neuronal use but show it also works in other cell types. Applying knockoff to synaptotagmin 1 (SYT1) results in acute disruption of this protein, resulting in loss of synchronous neurotransmitter release with a concomitant increase in the spontaneous release rate, measured optically. Thus, SYT1 is not only the proximal Ca

Indexed as

Synaptotagmin IAnimalsCells, CulturedHEK293 CellsHippocampusHumansMiceMice, KnockoutNeuronsNeurotransmitter AgentsRatsRats, Sprague-DawleyNeurotransmitter AgentsSynaptotagmin ISyt1 protein, mouseiGluSnFRKnockoffmouseneuroscienceratSynaptotagmin 1

Identifiers

PMID32515733
PMCPMC7282819

What OpenQuestion holds

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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.