Journal
TRAFFIC
Volume 15, Issue 4, Pages 418-432Publisher
WILEY
DOI: 10.1111/tra.12152
Keywords
actin; clathrin; endocytosis; myosin II
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Funding
- NIH [R21 MH081260, R21EB9776, L-090937, P20RR016440]
- Bakewell Neuroimaging Core
- Bakewell Family Foundation
- National Institutes of Health Neuroscience Blueprint Interdisciplinary Center Core Grant [P30 (NS057105)]
- NHLB (DIR)
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Variable requirements for actin during clathrin-mediated endocytosis (CME) may be related to regional or cellular differences in membrane tension. To compensate, local regulation of force generation may be needed to facilitate membrane curving and vesicle budding. Force generation is assumed to occur primarily through actin polymerization. Here we examine the role of myosin II using loss of function experiments. Our results indicate that myosin II acts on cortical actin scaffolds primarily in the plane of the plasma membrane (bottom arrow) to generate changes that are critical for enhancing CME progression.
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