ArticleProceedings of the National Academy of Sciences of the United States of America2013
Distinct biophysical mechanisms of focal adhesion kinase mechanoactivation by different extracellular matrix proteins.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers.
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Who cites it
112 citing papers in PubMed, 192 citations in OpenAlex.
- Mechanical regulation of cell memory.Nature structural & molecular biology · 2026Review
- FOS Regulates Myogenic and Adipogenic Differentiation via Extracellular Matrix Signaling.Journal of agricultural and food chemistry · 2026Article
- Deformability screening identifies NUDT5 as a mediator of cellular mechanobiology.bioRxiv : the preprint server for biology · 2026Article
- Impact of Stiffness and Cell-Binding Motif Availability on the Cell-Specific Response to Collagen-Based Macromolecular Materials.Biomacromolecules · 2026Article
- Cardiac mechanotransduction from development to disease.APL bioengineering · 2026Review
- Mechanobiology of the Hippo-YAP Signaling Network.Cold Spring Harbor perspectives in biology · 2026Article
- Stiff matrix-induced KRTAP2-3 expression suppresses ciliogenesis via actin tension-driven chromatin remodeling.Cell death & disease · 2026Article
- Disarming cancer resistance: FAK as a therapeutic target.Trends in cancer · 2026Review
- Integrin α2: mode of regulation and functioning in the metastatic cancer cascade.Journal of translational medicine · 2026Review
- Melanocyte differentiation and mechanosensation are differentially modulated by distinct extracellular matrix proteins.EMBO reports · 2025Article
- Mechanochemical waves in focal adhesions during cell migration.Science advances · 2025Article
- Article
- Thermally Cured Gelatin-Methacryloyl Hydrogels Form Mechanically Modulating Platforms for Cell Studies.Biomacromolecules · 2025Article
- A Live Cell Imaging-Compatible Bioreactor for the Interrogation of Cellular Responses to Modulated Flow Conditions.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Phospho-regulated tethering of focal adhesion kinase to vinculin links force transduction to focal adhesion signaling.Cell communication and signaling : CCS · 2025Article
- Acoustic modulation of mechanosensitive genes and adipocyte differentiation.Communications biology · 2025Article
- Focal adhesion kinase signaling - tumor vulnerabilities and clinical opportunities.Journal of cell science · 2024Review
- TiOAdvanced materials (Deerfield Beach, Fla.) · 2024Article
- Culture substrate stiffness impacts human myoblast contractility-dependent proliferation and nuclear envelope wrinkling.Journal of cell science · 2024Article
- Shaping Oncogenic Microenvironments: Contribution of Fibronectin.Frontiers in cell and developmental biology · 2024Review
52 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 7 institutions in 3 countries.
Funding
Abstract
Matrix mechanics controls cell fate by modulating the bonds between integrins and extracellular matrix (ECM) proteins. However, it remains unclear how fibronectin (FN), type 1 collagen, and their receptor integrin subtypes distinctly control force transmission to regulate focal adhesion kinase (FAK) activity, a crucial molecular signal governing cell adhesion/migration. Here we showed, using a genetically encoded FAK biosensor based on fluorescence resonance energy transfer, that FN-mediated FAK activation is dependent on the mechanical tension, which may expose its otherwise hidden FN synergy site to integrin α5. In sharp contrast, the ligation between the constitutively exposed binding motif of type 1 collagen and its receptor integrin α2 was surprisingly tension-independent to induce sufficient FAK activation. Although integrin α subunit determines mechanosensitivity, the ligation between α subunit and the ECM proteins converges at the integrin β1 activation to induce FAK activation. We further discovered that the interaction of the N-terminal protein 4.1/ezrin/redixin/moesin basic patch with phosphatidylinositol 4,5-biphosphate is crucial during cell adhesion to maintain the FAK activation from the inhibitory effect of nearby protein 4.1/ezrin/redixin/moesin acidic sites. Therefore, different ECM proteins either can transmit or can shield from mechanical forces to regulate cellular functions, with the accessibility of ECM binding motifs by their specific integrin α subunits determining the biophysical mechanisms of FAK activation during mechanotransduction.
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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.