ArticleMolecular biology of the cell2008
Munc18-1 is critical for plasma membrane localization of syntaxin1 but not of SNAP-25 in PC12 cells.
Article in Molecular biology of the cell, 2008. 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, 98 citations in OpenAlex.
- Functional differences of Munc18 isoforms reflect their affinities for the exocytosis site.Cellular and molecular life sciences : CMLS · 2026Article
- Munc18-1 is crucial for photoreceptor function, survival and regulation of syntaxin-3 localization and expression.Scientific reports · 2026Article
- The DDHD2-STXBP1 interaction mediates long-term memory via generation of saturated free fatty acids.The EMBO journal · 2024Article
- Double mutation of open syntaxin and UNC-18 P334A leads to excitatory-inhibitory imbalance and impairs multiple aspects ofbioRxiv : the preprint server for biology · 2023Article
- 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
- Article
- Novel Roles for Diacylglycerol in Synaptic Vesicle Priming and Release Revealed by Complete Reconstitution of Core Protein Machinery.bioRxiv : the preprint server for biology · 2023Article
- SNARE Proteins in Synaptic Vesicle Fusion.Advances in neurobiology · 2023Article
- The Role of Tomosyn in the Regulation of Neurotransmitter Release.Advances in neurobiology · 2023Article
- Article
- Presynaptic Short-Term Plasticity Persists in the Absence of PKC Phosphorylation of Munc18-1.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Munc13 binds and recruits SNAP25 to chaperone SNARE complex assembly.FEBS letters · 2021Article
- Exploring the Two Coupled Conformational Changes That Activate the Munc18-1/Syntaxin-1 Complex.Frontiers in molecular neuroscience · 2021Article
- Open syntaxin overcomes exocytosis defects of diverse mutants in C. elegans.Nature communications · 2020Article
- Munc13 activates the Munc18-1/syntaxin-1 complex and enables Munc18-1 to prime SNARE assembly.The EMBO journal · 2020Article
- CaTrends in cell biology · 2018Review
- Bi-Allelic Mutations in STXBP2 Reveal a Complementary Role for STXBP1 in Cytotoxic Lymphocyte Killing.Frontiers in immunology · 2018Article
- BDNF-TrkB Signaling Coupled to nPKCε and cPKCβI Modulate the Phosphorylation of the Exocytotic Protein Munc18-1 During Synaptic Activity at the Neuromuscular Junction.Frontiers in molecular neuroscience · 2018Article
- MUNC18-1 gene abnormalities are involved in neurodevelopmental disorders through defective cortical architecture during brain development.Acta neuropathologica communications · 2017Article
- UNC-18 and Tomosyn Antagonistically Control Synaptic Vesicle Priming Downstream of UNC-13 inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Although Munc18-1 was originally identified as a syntaxin1-interacting protein, the physiological significance of this interaction remains unclear. In fact, recent studies of Munc18-1 mutants have suggested that Munc18-1 plays a critical role for docking of secretory vesicles, independent of syntaxin1 regulation. Here we investigated the role of Munc18-1 in syntaxin1 localization by generating stable neuroendocrine cell lines in which Munc18-1 was strongly down-regulated. In these cells, the secretion capability, as well as the docking of dense-core vesicles, was significantly reduced. More importantly, not only was the expression level of syntaxin1 reduced, but the localization of syntaxin1 at the plasma membrane was also severely perturbed. The mislocalized syntaxin1 resided primarily in the perinuclear region of the cells, in which it was highly colocalized with Secretogranin II, a marker protein for dense-core vesicles. In contrast, the expression level and the plasma membrane localization of SNAP-25 were not affected. Furthermore, the syntaxin1 localization and the secretion capability were restored upon transfection-mediated reintroduction of Munc18-1. Our results indicate that endogenous Munc18-1 plays a critical role for the plasma membrane localization of syntaxin1 in neuroendocrine cells and therefore necessitates the interpretation of Munc18-1 mutant phenotypes to be in terms of mislocalized syntaxin1.
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