ArticleJournal of cell science2018
Epidermal growth factor receptor and integrins control force-dependent vinculin recruitment to E-cadherin junctions.
Article in Journal of cell science, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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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
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
19 citing papers in PubMed, 32 citations in OpenAlex.
- Beyond the membrane: rethinking EGFR signaling in physiology and cancer.Cellular and molecular life sciences : CMLS · 2026Review
- Epidermal growth factor receptor is an essential component in E-cadherin force transduction complexes.Journal of cell science · 2025Article
- Cadherins and growth factor receptors - ligand-selective mechano-switches at cadherin junctions.Journal of cell science · 2025Article
- Regulation of intercellular viscosity by E-cadherin-dependent phosphorylation of EGFR in collective cell migration.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Emerging roles and mechanisms of ERK pathway mechanosensing.Cellular and molecular life sciences : CMLS · 2023Review
- Interplay between EGFR, E-cadherin, and PTP1B in epidermal homeostasis.Tissue barriers · 2023Review
- Expression of JCAD and EGFR in Perineurial Cell-Cell Junctions of Human Inferior Alveolar Nerve.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2023Article
- The Regenerative Power of Stem Cells: Treating Bleomycin-Induced Lung Fibrosis.Stem cells and cloning : advances and applications · 2023Review
- Cadherins and catenins in cancer: connecting cancer pathways and tumor microenvironment.Frontiers in cell and developmental biology · 2023Review
- Extracellular matrix regulates force transduction at VE-cadherin junctions.Molecular biology of the cell · 2022Article
- Mechanical disruption of E-cadherin complexes with epidermal growth factor receptor actuates growth factor-dependent signaling.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Article
- The Cross-Talk Between EGFR and E-Cadherin.Frontiers in cell and developmental biology · 2021Review
- Mechanoregulation of Vascular Endothelial Growth Factor Receptor 2 in Angiogenesis.Frontiers in cardiovascular medicine · 2021Review
- Abl and Canoe/Afadin mediate mechanotransduction at tricellular junctions.Science (New York, N.Y.) · 2020Article
- New perspectives on integrin-dependent adhesions.Current opinion in cell biology · 2020Review
- Force transduction by cadherin adhesions in morphogenesis.F1000Research · 2019Review
- Distinct roles of VE-cadherin for development and maintenance of specific lymph vessel beds.The EMBO journal · 2018Article
- Modeling Tissue Polarity in Context.Journal of molecular biology · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
This study reports novel findings that link E-cadherin (also known as CDH1)-mediated force-transduction signaling to vinculin targeting to intercellular junctions via epidermal growth factor receptor (EGFR) and integrins. These results build on previous findings that demonstrated that mechanically perturbed E-cadherin receptors activate phosphoinositide 3-kinase and downstream integrins in an EGFR-dependent manner. Results of this study show that this EGFR-mediated kinase cascade controls the force-dependent recruitment of vinculin to stressed E-cadherin complexes - a key early signature of cadherin-based mechanotransduction. Vinculin targeting requires its phosphorylation at tyrosine 822 by Abl family kinases (hereafter Abl), but the origin of force-dependent Abl activation had not been identified. We now present evidence that integrin activation, which is downstream of EGFR signaling, controls Abl activation, thus linking E-cadherin to Abl through a mechanosensitive signaling network. These findings place EGFR and integrins at the center of a positive-feedback loop, through which force-activated E-cadherin signals regulate vinculin recruitment to cadherin complexes in response to increased intercellular tension.This article has an associated First Person interview with the first author of the paper.
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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.