ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Weak and Tunable Adhesion-Clutch Drives Rapid Cell Migration and Glioblastoma Invasion.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
The trial behind it
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Who cites it
5 citing papers in PubMed.
- The novel [RSC advances · 2026Article
- Mechanical polarity links adhesion-regulated protrusions to directional stability in glioblastoma cell migration.PLoS computational biology · 2026Article
- L1CAM Promotes the Infiltrative Properties of Patient-Derived Glioblastoma Cells.Cancer science · 2026Article
- Structurally exclusive Teneurin complexes orchestrate divergent programs in early cortical development.Nature communications · 2026Article
- Weak and Tunable Adhesion-Clutch Drives Rapid Cell Migration and Glioblastoma Invasion.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
Corrections and comments
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Authors and funding
16 authors.
Funding
Abstract
To move forward, cells must exert backward forces against their surrounding environment. Recent studies have highlighted the importance of integrin-independent forces for cell migration; however, the molecular machinery that exerts forces remains unclear. This study shows that the clutch-linker molecule shootin1 and the cell adhesion molecule L1 transmit the backward force of treadmilling actin filaments to the environment, enabling rapid dendritic cell migration. Notably, shootin1 and L1 transmit weak traction forces, up to ∼100 times weaker than integrin-based forces, by constituting an integrin-independent slippery adhesion-clutch. This adhesion-clutch is tunable in response to the chemoattractant CCL19 and the adhesive ligand laminin, thereby enabling chemotaxis and haptokinesis. Furthermore, aberrant activity of this adhesion-clutch enhances glioblastoma cell invasion. The results show that the weak adhesion-clutch is well-suited for rapid cell migration, without forming strong adhesions that impede cell motility, and provides a potential target for inhibiting abnormal tumor invasion.
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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.