ArticleCellular and molecular neurobiology2009
Expression of the dominant-negative tail of myosin Va enhances exocytosis of large dense core vesicles in neurons.
Article in Cellular and molecular neurobiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 26 citations in OpenAlex.
- Roles of molecular motors in insulin-secreting beta cells.Current opinion in cell biology · 2025Review
- Nanoelectrochemistry reveals how presynaptic neurons regulate vesicle release to sustain synaptic plasticity under repetitive stimuli.Chemical science · 2024Article
- Endoplasmic reticulum visits highly active spines and prevents runaway potentiation of synapses.Nature communications · 2020Article
- Article
- The molecular motor Myosin Va interacts with the cilia-centrosomal protein RPGRIP1L.Scientific reports · 2017Article
- Regulation of cellular communication by signaling microdomains in the blood vessel wall.Pharmacological reviews · 2014Review
- Functions of class V myosins in neurons.The Journal of biological chemistry · 2013Review
- Multiple roles for the actin cytoskeleton during regulated exocytosis.Cellular and molecular life sciences : CMLS · 2013Review
- Actomyosin II contractility expels von Willebrand factor from Weibel-Palade bodies during exocytosis.The Journal of cell biology · 2011Article
- Myosin-Va transports the endoplasmic reticulum into the dendritic spines of Purkinje neurons.Nature cell biology · 2011Article
- Article
- MARCKS and related chaperones bind to unconventional myosin V isoforms in airway epithelial cells.American journal of respiratory cell and molecular biology · 2010Article
- Dominant-negative myosin Va impairs retrograde but not anterograde axonal transport of large dense core vesicles.Cellular and molecular neurobiology · 2010Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Regulated exocytosis of secretory vesicles is a fundamental process in neurotransmission and the release of hormones and growth factors. The F-actin-binding motor protein myosin Va was recently shown to be involved in exocytosis of peptide-containing large dense core vesicles of neuroendocrine cells. It has not previously been discussed whether it plays a similar role in neurons. We performed live-cell imaging of cultured hippocampal neurons to measure the exocytosis of large dense core vesicles containing fluorescently labelled neuropeptide Y. To address the role of myosin Va in this process, neurons were transfected with the dominant-negative tail domain of myosin Va (myosinVa-tail). Under control conditions, about 0.75% of the labelled large dense core vesicles underwent exocytosis during 5 min of stimulation. This value was doubled to 1.80% of the vesicles when myosinVa-tail was expressed. Depolymerization of F-actin using latrunculin B resulted in a similar increase in exocytosis in both control and myosinVa-tail expressing cells. Interestingly, the increase in exocytosis caused by myosinVa-tail expression was completely abolished in the presence of KN-62, an inhibitor of calcium-calmodulin-dependent kinase II. We suggest that myosinVa-tail causes the liberation of large dense core vesicles from the actin cytoskeleton, leading to an increase in exocytosis in the cultured hippocampal neurons.
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