ArticleThe EMBO journal2013
CDC42 switches IRSp53 from inhibition of actin growth to elongation by clustering of VASP.
Article in The EMBO journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
What it found
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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
65 citing papers in PubMed, 135 citations in OpenAlex.
- Mechanisms of active wetting and fluidification in epithelial cell collectives.Nature materials · 2026Article
- Breaking cellular boundaries: molecular mechanisms of tunneling nanotube formation and fusion.Biochemical Society transactions · 2026Review
- Protrusion-Derived Extracellular Vesicles (PD-EVs) and Their Diverse Origins: Key Players in Cellular Communication, Cancer Progression, and T Cell Modulation.Biology of the cell · 2025Review
- Intercellular adhesion boots collective cell migration through elevated membrane tension.Nature communications · 2025Article
- NHSL3 controls single and collective cell migration through two distinct mechanisms.Nature communications · 2025Article
- Probing the protrusions: lamellipodia and filopodia in cancer invasion and beyond.Mechanobiology in medicine · 2024Review
- BIN1 regulates actin-membrane interactions during IRSp53-dependent filopodia formation.Communications biology · 2024Article
- Filopodial protrusion driven by density-dependent Ena-TOCA-1 interactions.Journal of cell science · 2024Article
- Tunneling Nanotubes: The Cables for Viral Spread and Beyond.Results and problems in cell differentiation · 2024Review
- Tunnelling nanotube formation is driven by Eps8/IRSp53-dependent linear actin polymerization.The EMBO journal · 2023Article
- Reconstitution of the transition from a lamellipodia- to filopodia-like actin network with purified proteins.European journal of cell biology · 2023Article
- Fusion pore dynamics of large secretory vesicles define a distinct mechanism of exocytosis.The Journal of cell biology · 2023Article
- Article
- Molecular Relay Stations in Membrane Nanotubes: IRSp53 Involved in Actin-Based Force Generation.International journal of molecular sciences · 2023Article
- Liquid-like VASP condensates drive actin polymerization and dynamic bundling.Nature physics · 2023Article
- Article
- Membrane reshaping by protein condensates.Biochimica et biophysica acta. Biomembranes · 2023Review
- Macrophages modulate stiffness-related foreign body responses through plasma membrane deformation.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Ena/VASP clustering at microspike tips involves lamellipodin but not I-BAR proteins, and absolutely requires unconventional myosin-X.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- SARS-CoV-2 replication in airway epithelia requires motile cilia and microvillar reprogramming.Cell · 2023Article
5 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors at 7 institutions in 5 countries.
Funding
Abstract
Filopodia explore the environment, sensing soluble and mechanical cues during directional motility and tissue morphogenesis. How filopodia are initiated and spatially restricted to specific sites on the plasma membrane is still unclear. Here, we show that the membrane deforming and curvature sensing IRSp53 (Insulin Receptor Substrate of 53 kDa) protein slows down actin filament barbed end growth. This inhibition is relieved by CDC42 and counteracted by VASP, which also binds to IRSp53. The VASP:IRSp53 interaction is regulated by activated CDC42 and promotes high-density clustering of VASP, which is required for processive actin filament elongation. The interaction also mediates VASP recruitment to liposomes. In cells, IRSp53 and VASP accumulate at discrete foci at the leading edge, where filopodia are initiated. Genetic removal of IRSp53 impairs the formation of VASP foci, filopodia and chemotactic motility, while IRSp53 null mice display defective wound healing. Thus, IRSp53 dampens barbed end growth. CDC42 activation inhibits this activity and promotes IRSp53-dependent recruitment and clustering of VASP to drive actin assembly. These events result in spatial restriction of VASP filament elongation for initiation of filopodia during cell migration, invasion, and tissue repair.
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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.