ArticleJournal of cell science2016
The role of myosin 1c and myosin 1b in surfactant exocytosis.
Article in Journal of cell science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 33 citations in OpenAlex.
- Pathogenic mechanism of the PLS1 gene variant in hearing loss and functional validation in a zebrafish model.Scientific reports · 2026Article
- Myosin Class I Genes Follow a Cell Type-Specific Transcription Pattern in Human Haematopoietic Cell Lines.International journal of molecular sciences · 2026Article
- Roles of myosin 1e and the actin cytoskeleton in kidney functions and familial kidney disease.Cytoskeleton (Hoboken, N.J.) · 2024Review
- Myosin-1C augments endothelial secretion of von Willebrand factor by linking contractile actomyosin machinery to the plasma membrane.Blood advances · 2024Article
- Myo1c drives actin-dependent VWF expulsion from EC WPBs.Blood advances · 2024Article
- Fusion pore dynamics of large secretory vesicles define a distinct mechanism of exocytosis.The Journal of cell biology · 2023Article
- Myo1d promotes alpha-synuclein transfer from brain microvascular endothelial cells to pericytes through tunneling nanotubes.iScience · 2023Article
- Class I Myosins, molecular motors involved in cell migration and cancer.Cell adhesion & migration · 2022Article
- MYO1H is a novel candidate gene for autosomal dominant pure hereditary spastic paraplegia.Molecular genetics and genomics : MGG · 2022Article
- Review
- Actin and Myosin in Non-Neuronal Exocytosis.Cells · 2020Review
- Basic-hydrophobic sites are localized in conserved positions inside and outside of PH domains and affect localization ofMolecular biology of the cell · 2020Article
- Downregulation of MYO1C mediated by cepharanthine inhibits autophagosome-lysosome fusion through blockade of the F-actin network.Journal of experimental & clinical cancer research : CR · 2019Article
- Interaction of microtubules and actin during the post-fusion phase of exocytosis.Scientific reports · 2019Article
- An Interaction Network of the Human SEPT9 Established by Quantitative Mass Spectrometry.G3 (Bethesda, Md.) · 2019Article
- Myosin-1c promotes E-cadherin tension and force-dependent recruitment of α-actinin to the epithelial cell junction.Journal of cell science · 2018Article
- Myosin-1 inhibition by PClP affects membrane shape, cortical actin distribution and lipid droplet dynamics in early Zebrafish embryos.PloS one · 2017Article
- Myosin-I molecular motors at a glance.Journal of cell science · 2016Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Actin and actin-associated proteins have a pivotal effect on regulated exocytosis in secretory cells and influence pre-fusion as well as post-fusion stages of exocytosis. Actin polymerization on secretory granules during the post-fusion phase (formation of an actin coat) is especially important in cells with large secretory vesicles or poorly soluble secretions. Alveolar type II (ATII) cells secrete hydrophobic lipo-protein surfactant, which does not easily diffuse from fused vesicles. Previous work showed that compression of actin coat is necessary for surfactant extrusion. Here, we investigate the role of class 1 myosins as possible linkers between actin and membranes during exocytosis. Live-cell microscopy showed translocation of fluorescently labeled myosin 1b and myosin 1c to the secretory vesicle membrane after fusion. Myosin 1c translocation was dependent on its pleckstrin homology domain. Expression of myosin 1b and myosin 1c constructs influenced vesicle compression rate, whereas only the inhibition of myosin 1c reduced exocytosis. These findings suggest that class 1 myosins participate in several stages of ATII cell exocytosis and link actin coats to the secretory vesicle membrane to influence vesicle compression.
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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 OpenQuestion graph.