ArticleeLife2019
Multiple factors maintain assembled trans-SNARE complexes in the presence of NSF and αSNAP.
Article in eLife, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed.
- Guiding AlphaFold to predict how Munc13-1 opens Syntaxin-1.FEBS open bio · 2026Article
- Recent Structural Insights into the Molecular Architecture of Synapses.Advances in neurobiology · 2026Review
- Functional assembly of the Qc-SNARE with Sec18 and Sec17 on membranes.Molecular biology of the cell · 2026Article
- Complexin gains effective access to the assembling SNAREs via its membrane-binding C-terminal domain.The Journal of physiology · 2025Article
- Number and relative abundance of synaptic vesicles in functionally distinct priming states determine synaptic strength and short-term plasticity.The Journal of physiology · 2025Article
- Two successive oligomeric Munc13 assemblies scaffold vesicle docking and SNARE assembly to support neurotransmitter release.Nature communications · 2025Article
- Neurotransmission Sex Dichotomy in the Rat Hypothalamic Paraventricular Nucleus in Healthy and Infantile Spasm Model.Current issues in molecular biology · 2025Article
- Uncovering the Mechanisms of Intracellular Membrane Trafficking by Reconstituted Membrane Systems.Membranes · 2025Review
- Evaluation of synaptotagmin-1 action models by all-atom molecular dynamics simulations.FEBS open bio · 2025Article
- A lever hypothesis for Synaptotagmin-1 action in neurotransmitter release.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Complexin regulation of synaptic vesicle release: mechanisms in the central nervous system and specialized retinal ribbon synapses.Cell communication and signaling : CCS · 2024Review
- Exploring the structural dynamics of the vesicle priming machinery.Biochemical Society transactions · 2024Review
- A lever hypothesis for Synaptotagmin-1 action in neurotransmitter release.bioRxiv : the preprint server for biology · 2024Article
- SM protein Sly1 and a SNARE Habc domain promote membrane fusion through multiple mechanisms.The Journal of cell biology · 2024Article
- Beyond the MUN domain, Munc13 controls priming and depriming of synaptic vesicles.Cell reports · 2024Article
- Molecular mechanism underlying SNARE-mediated membrane fusion enlightened by all-atom molecular dynamics simulations.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Control of Munc13-1 Activity by Autoinhibitory Interactions Involving the Variable N-terminal Region.Journal of molecular biology · 2024Article
- Complexin has a dual synaptic function as checkpoint protein in vesicle priming and as a promoter of vesicle fusion.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Mechanisms of SNARE proteins in membrane fusion.Nature reviews. Molecular cell biology · 2024Review
- Control of Munc13-1 Activity by Autoinhibitory Interactions Involving the Variable N-terminal Region.bioRxiv : the preprint server for biology · 2024Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Neurotransmitter release requires formation of trans-SNARE complexes between the synaptic vesicle and plasma membranes, which likely underlies synaptic vesicle priming to a release-ready state. It is unknown whether Munc18-1, Munc13-1, complexin-1 and synaptotagmin-1 are important for priming because they mediate trans-SNARE complex assembly and/or because they prevent trans-SNARE complex disassembly by NSF-αSNAP, which can lead to de-priming. Here we show that trans-SNARE complex formation in the presence of NSF-αSNAP requires both Munc18-1 and Munc13-1, as proposed previously, and is facilitated by synaptotagmin-1. Our data also show that Munc18-1, Munc13-1, complexin-1 and likely synaptotagmin-1 contribute to maintaining assembled trans-SNARE complexes in the presence of NSF-αSNAP. We propose a model whereby Munc18-1 and Munc13-1 are critical not only for mediating vesicle priming but also for precluding de-priming by preventing trans-SNARE complex disassembly; in this model, complexin-1 also impairs de-priming, while synaptotagmin-1 may assist in priming and hinder de-priming.
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Registered trials
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.