ArticleThe EMBO journal2024
Ezrin, radixin, and moesin are dispensable for macrophage migration and cellular cortex mechanics.
Article in The EMBO journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed.
- ERM Inhibition Confers Ferroptosis Resistance through ROS-Induced NRF2 Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- SARS-CoV-2 S assembly into virions facilitated by host ERM proteins.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Immune-related actinopathies at the cross-road of immunodeficiency, autoimmunity and autoinflammation.Nature reviews. Immunology · 2026Review
- Gigantol Preserves Lens Biophysical Homeostasis by Restoring Cytoskeletal Integrity and Membrane Fluidity in a Diabetic Cataract Model.International journal of molecular sciences · 2026Article
- Mechanical control of osteoclast fusion by membrane-cortex attachment and BAR proteins.The Journal of cell biology · 2025Article
- Tension-induced adhesion mode switching: the interplay between focal adhesions and clathrin-containing adhesion complexes.bioRxiv : the preprint server for biology · 2024Article
Corrections and comments
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Authors and funding
23 authors.
Funding
Abstract
The cellular cortex provides crucial mechanical support and plays critical roles during cell division and migration. The proteins of the ERM family, comprised of ezrin, radixin, and moesin, are central to these processes by linking the plasma membrane to the actin cytoskeleton. To investigate the contributions of the ERM proteins to leukocyte migration, we generated single and triple ERM knockout macrophages. Surprisingly, we found that even in the absence of ERM proteins, macrophages still form the different actin structures promoting cell migration, such as filopodia, lamellipodia, podosomes, and ruffles. Furthermore, we discovered that, unlike every other cell type previously investigated, the single or triple knockout of ERM proteins does not affect macrophage migration in diverse contexts. Finally, we demonstrated that the loss of ERMs in macrophages does not affect the mechanical properties of their cortex. These findings challenge the notion that ERMs are universally essential for cortex mechanics and cell migration and support the notion that the macrophage cortex may have diverged from that of other cells to allow for their uniquely adaptive cortical plasticity.
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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.