ArticleThe Journal of cell biology2014
Vinculin phosphorylation differentially regulates mechanotransduction at cell-cell and cell-matrix adhesions.
Article in The Journal of cell biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.
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Who cites it
99 citing papers in PubMed, 160 citations in OpenAlex.
- Vinculin mediates a dynamic signal flow underlying cardiac outflow tract development as revealed by single-cell and spatial transcriptomic analysis.Journal of advanced research · 2026Article
- ABL kinases regulate FGF signaling independent of CRK phosphorylation to prevent Peters anomaly type II.Nature communications · 2026Article
- Vinculin Y822 phosphorylation regulates adhesion remodeling during cardiomyocyte maturation.Journal of cell science · 2025Article
- Epidermal growth factor receptor is an essential component in E-cadherin force transduction complexes.Journal of cell science · 2025Article
- Epidermal stem cells control periderm injury repair via matrix-driven specialization of intercellular junctions.Nature communications · 2025Article
- E-Cadherin: A conductor of cellular signaling.Current opinion in cell biology · 2025Review
- Novel Electroactive Therapeutic Platforms for Cardiac Arrhythmia Management.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Distinct roles of protrusions and collagen deformation in collective invasion of cancer cell types.Biophysical journal · 2025Article
- Identification of c-Jun phosphorylation as a crucial mediator of complement activation in renal ischemia-reperfusion injury revealed by phosphoproteomics and functional validation.Molecular biology reports · 2025Article
- Focal adhesion in the tumour metastasis: from molecular mechanisms to therapeutic targets.Biomarker research · 2025Review
- Vinculin-Arp2/3 interaction inhibits branched actin assembly to control migration and proliferation.Life science alliance · 2025Article
- Coordination of Focal Adhesion Nanoarchitecture and Dynamics in Mechanosensing for Cardiomyoblast Differentiation.ACS applied materials & interfaces · 2025Article
- Shear stress-stimulated AMPK couples endothelial cell mechanics, metabolism and vasodilation.Journal of cell science · 2024Article
- Pushing boundaries: mechanisms enabling bacterial pathogens to spread between cells.Infection and immunity · 2024Review
- Alternative molecular mechanisms for force transmission at adherens junctions via β-catenin-vinculin interaction.Nature communications · 2024Article
- Examining the molecular mechanisms of topiramate in alleviating insulin resistance: A study on C2C12 myocytes and 3T3L-1 adipocytes.Endocrine · 2024Article
- Mechanical activation of VE-cadherin stimulates AMPK to increase endothelial cell metabolism and vasodilation.bioRxiv : the preprint server for biology · 2024Article
- N-cadherin and β1 integrin coordinately regulate growth plate cartilage architecture.Molecular biology of the cell · 2024Article
- Enhancing anti-tumor potential: low-intensity vibration suppresses osteosarcoma progression and augments MSCs' tumor-suppressive abilities.Theranostics · 2024Article
- Coupling during collective cell migration is controlled by a vinculin mechanochemical switch.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
39 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Cells experience mechanical forces throughout their lifetimes. Vinculin is critical for transmitting these forces, yet how it achieves its distinct functions at cell-cell and cell-matrix adhesions remains unanswered. Here, we show vinculin is phosphorylated at Y822 in cell-cell, but not cell-matrix, adhesions. Phosphorylation at Y822 was elevated when forces were applied to E-cadherin and was required for vinculin to integrate into the cadherin complex. The mutation Y822F ablated these activities and prevented cells from stiffening in response to forces on E-cadherin. In contrast, Y822 phosphorylation was not required for vinculin functions in cell-matrix adhesions, including integrin-induced cell stiffening. Finally, forces applied to E-cadherin activated Abelson (Abl) tyrosine kinase to phosphorylate vinculin; Abl inhibition mimicked the loss of vinculin phosphorylation. These data reveal an unexpected regulatory mechanism in which vinculin Y822 phosphorylation determines whether cadherins transmit force and provides a paradigm for how a shared component of adhesions can produce biologically distinct functions.
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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.