ArticleBiomaterials2024
FAK, vinculin, and talin control mechanosensitive YAP nuclear localization.
Article in Biomaterials, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 41 citations in OpenAlex.
- Review
- The Mechano-Immune-Vascular Activation Loop: An Integrative Conceptual Framework for Positive Feedback in Hypertension.International journal of molecular sciences · 2026Review
- Mechanobiology of orofacial tissues: principles, mechanisms, and therapeutic applications.International journal of oral science · 2026Review
- Mechanically Active Contractile Hydrogels for Skin Wound Repair.Gels (Basel, Switzerland) · 2026Review
- Dysregulated ITGA3/FAK/YAP axis mediates impaired alveolar type II epithelial cells function in COPD.Journal of advanced research · 2026Article
- Integrin-mediated mechanotransduction in the tumor microenvironment: macrophage-centered signaling mechanisms and immune remodeling.Journal of translational medicine · 2026Review
- FAK modulates immune response and fibroblast activation in biomaterial-induced fibrosis.Biomaterials · 2026Article
- Mechanical Signaling in the Microenvironment Regulates the Differentiation of Dental Pulp Stem Cells: A Novel Strategy For Pulp-Dentin Complex Regeneration.Stem cell reviews and reports · 2026Review
- Mechanical cues regulateMaterials today. Bio · 2026Article
- Transcriptomic and proteomic analysis of osteogenesis imperfecta disease-specific induced pluripotent stem cells.BMC medical genomics · 2026Article
- Nuclear Mechanotransduction Across the Metastatic Cascade: Decoding Spatiotemporal Heterogeneity in Cancer Dissemination.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Cell Mechanics in Cancer: Integrating Mechanotransduction Pathways Within the Tumor Microenvironment.Journal of cellular physiology · 2026Review
- UNC5B activates hepatic stellate cells and promotes liver fibrosis via FAK.Cell communication and signaling : CCS · 2026Article
- Mechanobiology of the Hippo-YAP Signaling Network.Cold Spring Harbor perspectives in biology · 2026Article
- Disarming cancer resistance: FAK as a therapeutic target.Trends in cancer · 2026Review
- ECM stiffness governs endothelial barrier integrity through YAP-mediated stabilization of ZO-1.Bioactive materials · 2026Article
- Hippo-YAP/TAZ signaling in inner ear development, injury, and regeneration: evidence synthesis and the biomechanical brake hypothesis.Frontiers in cell and developmental biology · 2026Review
- The talin1-p53 axis inhibits osteocyte senescence to promote bone mass and mediate skeletal adaptation to mechanical stimulation.Theranostics · 2026Article
- 3D-Printed Region-Specific Biomimetic Prosthesis for Enhancing Heterogeneous Double-Interface Integration of Bone-Prosthesis and Tendon-Prosthesis.Biomaterials research · 2026Article
- Interaction between m6A and YAP1 mechanotransduction pathways is essential for mechanical memory and matrix remodeling in pancreatic cancer.International journal of biological sciences · 2026Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Focal adhesions (FAs) are nanoscale complexes containing clustered integrin receptors and intracellular structural and signaling proteins that function as principal sites of mechanotransduction in part via promoting the nuclear translocation and activation of the transcriptional coactivator yes-associated protein (YAP). Knockdown of FA proteins such as focal adhesion kinase (FAK), talin, and vinculin can prevent YAP nuclear localization. However, the mechanism(s) of action remain poorly understood. Herein, we investigated the role of different functional domains in vinculin, talin, and FAK in regulating YAP nuclear localization. Using genetic or pharmacological inhibition of fibroblasts and human mesenchymal stem cells (hMSCs) adhering to deformable substrates, we find that disruption of vinculin-talin binding versus talin-FAK binding reduces YAP nuclear localization and transcriptional activity via different mechanisms. Disruption of vinculin-talin binding or knockdown of talin-1 reduces nuclear size, traction forces, and YAP nuclear localization. In contrast, disruption of the talin binding site on FAK or elimination of FAK catalytic activity did not alter nuclear size yet still prevented YAP nuclear localization and activity. These data support both nuclear tension-dependent and independent models for matrix stiffness-regulated YAP nuclear localization. Our results highlight the importance of vinculin-talin-FAK interactions at FAs of adherent cells, controlling YAP nuclear localization and activity.
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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.