ArticleThe Journal of biological chemistry2006
The stimulus-induced tyrosine phosphorylation of Munc18c facilitates vesicle exocytosis.
Article in The Journal of biological chemistry, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 52 citations in OpenAlex.
- GLUT4 On the move.The Biochemical journal · 2022Article
- Exocytosis Proteins: Typical and Atypical Mechanisms of Action in Skeletal Muscle.Frontiers in endocrinology · 2022Review
- Conventional and Unconventional Mechanisms by which Exocytosis Proteins Oversee β-cell Function and Protection.International journal of molecular sciences · 2021Review
- Article
- Application of High-Throughput Assays to Examine Phospho-Modulation of the Late Steps of Regulated Exocytosis.High-throughput · 2017Article
- Disruption of protein complexes containing protein phosphatase 2B and Munc18c reduces the secretion of von Willebrand factor from endothelial cells.Journal of thrombosis and haemostasis : JTH · 2017Article
- Exocytosis proteins as novel targets for diabetes prevention and/or remediation?American journal of physiology. Regulatory, integrative and comparative physiology · 2017Review
- Bariatric surgery in morbidly obese insulin resistant humans normalises insulin signalling but not insulin-stimulated glucose disposal.PloS one · 2015Article
- Doc2b serves as a scaffolding platform for concurrent binding of multiple Munc18 isoforms in pancreatic islet β-cells.The Biochemical journal · 2014Article
- Munc18c: a controversial regulator of peripheral insulin action.Trends in endocrinology and metabolism: TEM · 2014Review
- Doc2b enrichment enhances glucose homeostasis in mice via potentiation of insulin secretion and peripheral insulin sensitivity.Diabetologia · 2014Article
- Regulation of the SNARE-interacting protein Munc18c tyrosine phosphorylation in adipocytes by protein-tyrosine phosphatase 1B.Cell communication and signaling : CCS · 2013Article
- Doc2b is a key effector of insulin secretion and skeletal muscle insulin sensitivity.Diabetes · 2012Article
- Munc18-1 regulates first-phase insulin release by promoting granule docking to multiple syntaxin isoforms.The Journal of biological chemistry · 2012Article
- Gelsolin associates with the N terminus of syntaxin 4 to regulate insulin granule exocytosis.Molecular endocrinology (Baltimore, Md.) · 2012Article
- Modes of exocytosis and electrogenesis underlying canine biphasic insulin secretion.Frontiers in bioscience (Elite edition) · 2012Review
- Tyrosine phosphorylation of Munc18c on residue 521 abrogates binding to Syntaxin 4.BMC biochemistry · 2011Article
- Stimulus-induced S-nitrosylation of Syntaxin 4 impacts insulin granule exocytosis.The Journal of biological chemistry · 2011Article
- Munc18c phosphorylation by the insulin receptor links cell signaling directly to SNARE exocytosis.The Journal of cell biology · 2011Article
- Exocytosis mechanisms underlying insulin release and glucose uptake: conserved roles for Munc18c and syntaxin 4.American journal of physiology. Regulatory, integrative and comparative physiology · 2010Review
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Stimulus-induced tyrosine phosphorylation of Munc18c was investigated as a potential regulatory mechanism by which the Munc18c-Syntaxin 4 complex can be dissociated in response to divergent stimuli in multiple cell types. Use of [(32)P]orthophosphate incorporation, pervanadate treatment, and phosphotyrosine-specific antibodies demonstrated that Munc18c underwent tyrosine phosphorylation. Phosphorylation was apparent under basal conditions, but levels were significantly increased within 5 min of glucose stimulation in MIN6 beta cells. Tyrosine phosphorylation of Munc18c was also detected in 3T3L1 adipocytes and increased with insulin stimulation, suggesting that this may be a conserved mechanism. Syntaxin 4 binding to Munc18c decreased as Munc18c phosphorylation levels increased in pervanadate-treated cells, suggesting that phosphorylation dissociates the Munc18c-Syntaxin 4 complex. Munc18c phosphorylation was localized to the N-terminal 255 residues. Mutagenesis of one residue in this region, Y219F, significantly increased the affinity of Munc18c for Syntaxin 4, whereas mutation of three other candidate sites was without effect. Moreover, Munc18c-Y219F expression in MIN6 cells functionally inhibited glucose-stimulated SNARE complex formation and insulin granule exocytosis. These data support a novel and conserved mechanism for the dissociation of Munc18c-Syntaxin 4 complexes in a stimulus-dependent manner to facilitate the increase in Syntaxin 4-VAMP2 association and to promote vesicle/granule fusion.
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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.