ArticleeLife2018
A mechanism for exocytotic arrest by the Complexin C-terminus.
Article in eLife, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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The trial behind it
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Who cites it
13 citing papers in PubMed.
- A primordial synaptotagmin-independent function of complexin in regulated exocytosis.Nature communications · 2026Article
- Complexin gains effective access to the assembling SNAREs via its membrane-binding C-terminal domain.The Journal of physiology · 2025Article
- Complexin regulation of synaptic vesicle release: mechanisms in the central nervous system and specialized retinal ribbon synapses.Cell communication and signaling : CCS · 2024Review
- Article
- Stochastic RNA editing of the Complexin C-terminus within single neurons regulates neurotransmitter release.Cell reports · 2023Article
- Stochastic RNA editing of the Complexin C-terminus within single neurons regulates neurotransmitter release.bioRxiv : the preprint server for biology · 2023Article
- Complexin-1 regulated assembly of single neuronal SNARE complex revealed by single-molecule optical tweezers.Communications biology · 2023Article
- Complexin Membrane Interactions: Implications for Synapse Evolution and Function.Journal of molecular biology · 2023Review
- Synaptotagmin-7 places dense-core vesicles at the cell membrane to promote Munc13-2- and CaeLife · 2021Article
- Measurements of Exocytosis by Capacitance Recordings and Calcium Uncaging in Mouse Adrenal Chromaffin Cells.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Complexin Suppresses Spontaneous Exocytosis by Capturing the Membrane-Proximal Regions of VAMP2 and SNAP25.Cell reports · 2020Article
- Article
- Intrinsically disordered proteins in synaptic vesicle trafficking and release.The Journal of biological chemistry · 2019Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
ComplexinII (CpxII) inhibits non-synchronized vesicle fusion, but the underlying mechanisms have remained unclear. Here, we provide evidence that the far C-terminal domain (CTD) of CpxII interferes with SNARE assembly, thereby arresting tonic exocytosis. Acute infusion of a CTD-derived peptide into mouse chromaffin cells enhances synchronous release by diminishing premature vesicle fusion like full-length CpxII, indicating a direct, inhibitory function of the CTD that sets the magnitude of the primed vesicle pool. We describe a high degree of structural similarity between the CpxII CTD and the SNAP25-SN1 domain (C-terminal half) and show that the CTD peptide lowers the rate of SDS-resistant SNARE complex formation in vitro. Moreover, corresponding CpxII:SNAP25 chimeras do restore complexin's function and even 'superclamp' tonic secretion. Collectively, these results support a so far unrecognized clamping mechanism wherein the CpxII C-terminus hinders spontaneous SNARE complex assembly, enabling the build-up of a release-ready pool of vesicles for synchronized Ca
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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 Socratic graph.