ArticleJournal of cell science2017
Vimentin intermediate filaments control actin stress fiber assembly through GEF-H1 and RhoA.
Article in Journal of cell science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
118 citing papers in PubMed, 200 citations in OpenAlex.
- Article
- Vimentin remodeling in response to oxidants and electrophiles is modulated by pH.Science advances · 2026Article
- Integrin-mediated mechanotransduction in the tumor microenvironment: macrophage-centered signaling mechanisms and immune remodeling.Journal of translational medicine · 2026Review
- Mechanosensitive FHL2 tunes endothelial function via microtubule-actomyosin crosstalk.The EMBO journal · 2026Article
- Vimentin promotes collective cell migration through collagen networks via increased matrix remodeling and spheroid fluidity.Communications biology · 2026Article
- Vimentin molecular linkages with nesprin-3 enhance nuclear deformations by cell geometric constraints.Scientific reports · 2026Article
- Cell Mechanics in Cancer: Integrating Mechanotransduction Pathways Within the Tumor Microenvironment.Journal of cellular physiology · 2026Review
- Development of the relationship between tumor and mechanobiology over the past 30 years: a bibliometric analysis.Discover oncology · 2026Article
- Architects of the Developing Brain: Cytoskeleton-Organizing Molecules in Neurodevelopmental Disorders.Cells · 2026Review
- Modulating Vimentin: A Systems-Level Therapeutic Strategy for Sepsis and Complex Diseases.Life (Basel, Switzerland) · 2026Article
- Vimentin Intermediate Filaments: A Paradigm Shift From Static Structure to Dynamic Cytoplasmic Network.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026Review
- Migrasome as a novel organelle: Biogenesis, physiological functions, and therapeutic potential.Journal of translational internal medicine · 2026Article
- Plectin affects cell viscoelasticity at small and large deformations.Biophysical journal · 2026Article
- Targeting Tumor-Associated Macrophages to Reshape the Immuno-Mechanical Landscape: Molecular Mechanisms and Therapeutic Strategies.International journal of biological sciences · 2026Review
- Decoding Rho GTPase signalling networks in directed cell migration.Frontiers in cell and developmental biology · 2026Review
- Migrasomes: Emerging players in intercellular communication and disease pathogenesis (Review).Molecular medicine reports · 2026Review
- Aurora B maintains spherical shape of mitotic cells via simultaneously stabilizing myosin II and vimentin.Journal of molecular cell biology · 2025Article
- Vimentin cytoskeleton collapses in response to the small-molecule inhibitor of FH2 domains (SMIFH2)-induced electrophilic stress.Molecular biology of the cell · 2025Article
- RCC2 and CD24 cooperate to modulate prostate cancer progression through vimentin ubiquitination and β-catenin activation.The Journal of clinical investigation · 2025Article
- TM9SF1 inhibits colorectal cancer metastasis by targeting Vimentin for Tollip-mediated selective autophagic degradation.Cell death and differentiation · 2025Article
58 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
The actin and intermediate filament cytoskeletons contribute to numerous cellular processes, including morphogenesis, cytokinesis and migration. These two cytoskeletal systems associate with each other, but the underlying mechanisms of this interaction are incompletely understood. Here, we show that inactivation of vimentin leads to increased actin stress fiber assembly and contractility, and consequent elevation of myosin light chain phosphorylation and stabilization of tropomyosin-4.2 (see Geeves et al., 2015). The vimentin-knockout phenotypes can be rescued by re-expression of wild-type vimentin, but not by the non-filamentous 'unit length form' vimentin, demonstrating that intact vimentin intermediate filaments are required to facilitate the effects on the actin cytoskeleton. Finally, we provide evidence that the effects of vimentin on stress fibers are mediated by activation of RhoA through its guanine nucleotide exchange factor GEF-H1 (also known as ARHGEF2). Vimentin depletion induces phosphorylation of the microtubule-associated GEF-H1 on Ser886, and thereby promotes RhoA activity and actin stress fiber assembly. Taken together, these data reveal a new mechanism by which intermediate filaments regulate contractile actomyosin bundles, and may explain why elevated vimentin expression levels correlate with increased migration and invasion of cancer cells.
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Registered trials
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.