ArticleNature structural & molecular biology2010
Munc13 C2B domain is an activity-dependent Ca2+ regulator of synaptic exocytosis.
Article in Nature structural & molecular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It carries an expression of concern. Cited by 152 papers.
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Who cites it
152 citing papers in PubMed, 250 citations in OpenAlex.
- Thalamofrontal synaptic weakening underlies short-term memory deficits from adolescent NMDAR hypofunction.Science advances · 2026Article
- Guiding AlphaFold to predict how Munc13-1 opens Syntaxin-1.FEBS open bio · 2026Article
- Selective, genetically induced increase in synaptic vesicle priming.Science advances · 2026Article
- Munc13-1 couples DAG and CaScience advances · 2026Article
- The MO25 protein Pmo25 functions in contractile ring stability and Sid2 localization during cytokinesis.iScience · 2026Article
- Pathogenic UNC13A variants cause a neurodevelopmental syndrome by impairing synaptic function.Nature genetics · 2025Article
- Independently engaging protein tethers of different length enhance synaptic vesicle trafficking to the plasma membrane.The Journal of physiology · 2025Article
- Ageing-induced weakness of mouse NMJs is associated with reduced active zone density, synaptic event kinetics and presynaptic calcium entry.The Journal of physiology · 2025Article
- Roles of the MO25 protein Pmo25 in contractile-ring stability and localization of the NDR kinase Sid2 during cytokinesis.bioRxiv : the preprint server for biology · 2025Article
- 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 · 2025Article
- PI(4,5)PBiochimica et biophysica acta. Molecular and cell biology of lipids · 2025Review
- Article
- Single-Vesicle Microelectroanalysis Reveals the Role of PIP2 Phospholipid in Vesicle Opening Dynamics and Its Potential Role in Exocytosis.ACS omega · 2025Article
- Mechanisms that regulate the C1-C2B mutual inhibition control functional switch of UNC-13.eLife · 2025Article
- Beyond the MUN domain, Munc13 controls priming and depriming of synaptic vesicles.Cell reports · 2024Article
- Control of Munc13-1 Activity by Autoinhibitory Interactions Involving the Variable N-terminal Region.Journal of molecular biology · 2024Article
- Tomosyns attenuate SNARE assembly and synaptic depression by binding to VAMP2-containing template complexes.Nature communications · 2024Article
- Control of Munc13-1 Activity by Autoinhibitory Interactions Involving the Variable N-terminal Region.bioRxiv : the preprint server for biology · 2024Article
- Interpretation of presynaptic phenotypes of synaptic plasticity in terms of a two-step priming process.The Journal of general physiology · 2024Article
- 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 · 2023Article
92 more citing papers are in PubMed but not listed here.
Corrections and comments
- Expression of concern
Authors and funding
12 authors at 7 institutions in 2 countries.
Funding
Abstract
Munc13 is a multidomain protein present in presynaptic active zones that mediates the priming and plasticity of synaptic vesicle exocytosis, but the mechanisms involved remain unclear. Here we use biophysical, biochemical and electrophysiological approaches to show that the central C(2)B domain of Munc13 functions as a Ca(2+) regulator of short-term synaptic plasticity. The crystal structure of the C(2)B domain revealed an unusual Ca(2+)-binding site with an amphipathic alpha-helix. This configuration confers onto the C(2)B domain unique Ca(2+)-dependent phospholipid-binding properties that favor phosphatidylinositolphosphates. A mutation that inactivated Ca(2+)-dependent phospholipid binding to the C(2)B domain did not alter neurotransmitter release evoked by isolated action potentials, but it did depress release evoked by action-potential trains. In contrast, a mutation that increased Ca(2+)-dependent phosphatidylinositolbisphosphate binding to the C(2)B domain enhanced release evoked by isolated action potentials and by action-potential trains. Our data suggest that, during repeated action potentials, Ca(2+) and phosphatidylinositolphosphate binding to the Munc13 C(2)B domain potentiate synaptic vesicle exocytosis, thereby offsetting synaptic depression induced by vesicle depletion.
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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.