ArticleNature communications2015
Vinculin controls talin engagement with the actomyosin machinery.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 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
116 citing papers in PubMed, 223 citations in OpenAlex.
- Neutrophil Mechanosignaling Promotes Integrin Engagement With Endothelial Cells and Motility Within Inflamed Vessels.Frontiers in immunology · 2018Trial
- An integrin beta-1-anchored bicaudal C1-polycystin-1 module essential for tubular morphogenesis in polycystic kidney disease.iScience · 2026Article
- [Mechanobiology of peripheral nerve development: mechanical properties, sensing, and response].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2026Review
- Talin-tensin3 interactions regulate fibrillar adhesion formation and tensin3 phase separation.The Journal of cell biology · 2026Article
- Development of three-colour FRET cascade for force sensing of the putative RIAM-vinculin interaction in fibroblasts.Communications chemistry · 2025Article
- The variational modulus density theory explains mechanical responses of cell membranes and membrane crosslinkers.Scientific reports · 2025Article
- An overview of mechanical microenvironment and mechanotransduction in intervertebral disc degeneration.Experimental & molecular medicine · 2025Review
- The bidirectional interplay between RNA processing and mechanotransduction.Cell reports · 2025Review
- Kindlin Regulates Mechanosensitive Activation and Adhesion Assembly of Integrin beta6.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Actin Branching Regulates Cell Spreading and Force on Talin, but not Activation of YAP.Cellular and molecular bioengineering · 2025Article
- Consolidation of cell-ECM adhesion through direct talin-mediated actin linkage is essential for mouse embryonic morphogenesis.Communications biology · 2025Article
- Focal adhesion in the tumour metastasis: from molecular mechanisms to therapeutic targets.Biomarker research · 2025Review
- Biochemical and structural bases for talin ABSs-F-actin interactions.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Exploring focal adhesion data: dynamic parameter extraction from FRAP and FLAP experiments using chemical master equation.Frontiers in molecular biosciences · 2025Article
- Zymogen granule protein 16B (ZG16B) is a druggable epigenetic target to modulate the mammary extracellular matrix.Cancer science · 2025Article
- Integrin force loading rate in mechanobiology: From model to molecular measurement.QRB discovery · 2025Review
- Article
- Talin and vinculin combine their activities to trigger actin assembly.Nature communications · 2024Article
- Talin2 binds to non-muscle myosin IIa and regulates cell attachment and fibronectin secretion.Scientific reports · 2024Article
- Cellular stiffness sensing through talin 1 in tissue mechanical homeostasis.Science advances · 2024Article
56 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
13 authors at 7 institutions in 3 countries.
Funding
Abstract
The link between extracellular-matrix-bound integrins and intracellular F-actin is essential for cell spreading and migration. Here, we demonstrate how the actin-binding proteins talin and vinculin cooperate to provide this link. By expressing structure-based talin mutants in talin null cells, we show that while the C-terminal actin-binding site (ABS3) in talin is required for adhesion complex assembly, the central ABS2 is essential for focal adhesion (FA) maturation. Thus, although ABS2 mutants support cell spreading, the cells lack FAs, fail to polarize and exert reduced force on the surrounding matrix. ABS2 is inhibited by the preceding mechanosensitive vinculin-binding R3 domain, and deletion of R2R3 or expression of constitutively active vinculin generates stable force-independent FAs, although cell polarity is compromised. Our data suggest a model whereby force acting on integrin-talin complexes via ABS3 promotes R3 unfolding and vinculin binding, activating ABS2 and locking talin into an actin-binding configuration that stabilizes FAs.
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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.