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- W3112713031 abstract "Despite the well-established role of actin polymerization as a driving mechanism for cell protrusion, upregulated actin polymerization alone does not initiate protrusions. Using a combination of theoretical modeling and quantitative live-cell imaging experiments, we show that local depletion of actin-membrane links is needed for protrusion initiation. Specifically, we show that the actin-membrane linker ezrin is depleted prior to protrusion onset and that perturbation of ezrin's affinity for actin modulates protrusion frequency and efficiency. We also show how actin-membrane release works in concert with actin polymerization, leading to a comprehensive model for actin-driven shape changes. Actin-membrane release plays a similar role in protrusions driven by intracellular pressure. Thus, our findings suggest that protrusion initiation might be governed by a universal regulatory mechanism, whereas the mechanism of force generation determines the shape and expansion properties of the protrusion." @default.
- W3112713031 created "2020-12-21" @default.
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- W3112713031 date "2020-12-01" @default.
- W3112713031 modified "2023-10-15" @default.
- W3112713031 title "Actin-Membrane Release Initiates Cell Protrusions" @default.
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- W3112713031 doi "https://doi.org/10.1016/j.devcel.2020.11.024" @default.
- W3112713031 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7908823" @default.
- W3112713031 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/33308479" @default.
- W3112713031 hasPublicationYear "2020" @default.
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