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Updated: Dec 6, 2025

In Vitro Polymerization of F-actin on Early Endosomes
Published on: August 28, 2017
Unidirectional Regulation of Vimentin Intermediate Filaments to Caveolin-1
Xuemeng Shi1,2, Changyuan Fan2,3, Yaming Jiu1,2,3
1The Joint Program in Infection and Immunity, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou 510623, China.
Abstract:
Both the mechanosensitive vimentin cytoskeleton and endocytic caveolae contribute to various active processes such as cell migration, morphogenesis, and stress response. However, the crosstalk between these two systems has remained elusive. Here, we find that the subcellular expression between vimentin and caveolin-1 is mutual exclusive, and vimentin filaments physically arrest the cytoplasmic motility of caveolin-1 vesicles. Importantly, vimentin depletion increases the phosphorylation of caveolin-1 on site Tyr14, and restores the compromised cell migration rate and directionality caused by caveolin-1 deprivation. Moreover, upon hypo-osmotic shock, vimentin-knockout recovers the reduced intracellular motility of caveolin-1 vesicles. In contrary, caveolin-1 depletion shows no effect on the expression, phosphorylation (on sites Ser39, Ser56, and Ser83), distribution, solubility, and cellular dynamics of vimentin filaments. Taken together, our data reveals a unidirectional regulation of vimentin to caveolin-1, at least on the cellular level.
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