ArticleThe EMBO journal2012
Munc18-1 mutations that strongly impair SNARE-complex binding support normal synaptic transmission.
Article in The EMBO journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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.
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.
Who cites it
48 citing papers in PubMed, 78 citations in OpenAlex.
- Munc18-1 is crucial for photoreceptor function, survival and regulation of syntaxin-3 localization and expression.Scientific reports · 2026Article
- Non-Synaptic Function and Localization of Syntaxin-Binding Protein 1 in a Mouse Model of STXBP1-Related Epileptic Encephalopathy.Annals of neurology · 2026Article
- Pathogenic UNC13A variants cause a neurodevelopmental syndrome by impairing synaptic function.Nature genetics · 2025Article
- Structural remodeling of target-SNARE protein complexes by NSF enables synaptic transmission.Nature communications · 2025Article
- Structural remodeling of target-SNARE protein complexes by NSF enables synaptic transmission.bioRxiv : the preprint server for biology · 2025Article
- RIM and MUNC13 membrane-binding domains are essential for neuropeptide secretion.The Journal of cell biology · 2025Article
- Functional Roles of UNC-13/Munc13 and UNC-18/Munc18 in Neurotransmission.Advances in neurobiology · 2023Review
- SNARE Proteins in Synaptic Vesicle Fusion.Advances in neurobiology · 2023Article
- Genetic disorders of neurotransmitter release machinery.Frontiers in synaptic neuroscience · 2023Review
- Differential axonal trafficking of Neuropeptide Y-, LAMP1-, and RAB7-tagged organelles in vivo.eLife · 2022Article
- Energetics, kinetics, and pathways of SNARE assembly in membrane fusion.Critical reviews in biochemistry and molecular biology · 2022Review
- Article
- Reexamination of N-terminal domains of syntaxin-1 in vesicle fusion from central murine synapses.eLife · 2021Article
- Chaperoning SNARE Folding and Assembly.Annual review of biochemistry · 2021Review
- STXBP1 encephalopathies: Clinical spectrum, disease mechanisms, and therapeutic strategies.Journal of neurochemistry · 2021Review
- Functional analysis of epilepsy-associated variants in STXBP1/Munc18-1 using humanized Caenorhabditis elegans.Epilepsia · 2020Article
- Article
- Fbxo41 Promotes Disassembly of Neuronal Primary Cilia.Scientific reports · 2019Article
- Article
- The N-peptide-binding mode is critical to Munc18-1 function in synaptic exocytosis.The Journal of biological chemistry · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Synaptic transmission depends critically on the Sec1p/Munc18 protein Munc18-1, but it is unclear whether Munc18-1 primarily operates as a integral part of the fusion machinery or has a more upstream role in fusion complex assembly. Here, we show that point mutations in Munc18-1 that interfere with binding to the free Syntaxin1a N-terminus and strongly impair binding to assembled SNARE complexes all support normal docking, priming and fusion of synaptic vesicles, and normal synaptic plasticity in munc18-1 null mutant neurons. These data support a prevailing role of Munc18-1 before/during SNARE-complex assembly, while its continued association to assembled SNARE complexes is dispensable for synaptic transmission.
Indexed as
Identifiers
What OpenQuestion holds
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.