ArticleThe Journal of biological chemistry2013
α-Catenin and vinculin cooperate to promote high E-cadherin-based adhesion strength.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers.
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Who cites it
106 citing papers in PubMed, 178 citations in OpenAlex.
- Actomyosin-dependent assembly of the mechanosensitive machinery from adherens junctions triggers actin polymerization and organization.Science advances · 2026Article
- Genetically engineered ESC-derived embryos reveal Vinculin-dependent force responses required for mammalian neural tube closure.bioRxiv : the preprint server for biology · 2025Article
- UBE2O-mediated ubiquitylation directs cytoplasmic CTNNA1 to promote cell-to-ECM adhesions.EMBO reports · 2025Article
- CRB3 and NF2 orchestrate cytoskeletal dynamics to control epithelial barrier assembly.JCI insight · 2025Article
- α-catenin phosphorylation is actomyosin-sensitive and required for epithelial barrier functions through Afadin.bioRxiv : the preprint server for biology · 2025Article
- Neighbor cells restrain furrowing during Xenopus epithelial cytokinesis.Developmental cell · 2025Article
- Mechanical strengthening of cell-cell adhesion during mouse embryo compaction.Biophysical journal · 2025Article
- α-Catenin force-sensitive binding and sequestration of LZTS2 leads to cytokinesis failure.The Journal of cell biology · 2025Article
- Crb3 and NF2: A dynamic duo that controls assembly of the apical junctions and barrier function via Rho/ROCK signaling.bioRxiv : the preprint server for biology · 2025Article
- Mechanosensitive recruitment of Vinculin maintains junction integrity and barrier function at epithelial tricellular junctions.Current biology : CB · 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
- α-catenin middle- and actin-binding domain unfolding mutants differentially impact epithelial strength and sheet migration.Molecular biology of the cell · 2024Article
- Nonlobular Invasive Breast Carcinomas with Biallelic Pathogenic CDH1 Somatic Alterations: A Histologic, Immunophenotypic, and Genomic Characterization.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2024Article
- Vinculin is essential for sustaining normal levels of endogenous forces at cell-cell contacts.Biophysical journal · 2023Article
- E-cadherin adhesion dynamics as revealed by an accelerated force ramp are dependent upon the presence of α-catenin.Biochemical and biophysical research communications · 2023Article
- Tumour follower cells: A novel driver of leader cells in collective invasion (Review).International journal of oncology · 2023Review
- Push-pull mechanics of E-cadherin ectodomains in biomimetic adhesions.Biophysical journal · 2023Article
- MAP4K4 regulates forces at cell-cell and cell-matrix adhesions to promote collective cell migration.Life science alliance · 2023Article
- α-catenin mechanosensitivity as a route to cytokinesis failure through sequestration of LZTS2.bioRxiv : the preprint server for biology · 2023Article
46 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Maintaining cell cohesiveness within tissues requires that intercellular adhesions develop sufficient strength to support traction forces applied by myosin motors and by neighboring cells. Cadherins are transmembrane receptors that mediate intercellular adhesion. The cadherin cytoplasmic domain recruits several partners, including catenins and vinculin, at sites of cell-cell adhesion. Our study used force measurements to address the role of αE-catenin and vinculin in the regulation of the strength of E-cadherin-based adhesion. αE-catenin-deficient cells display only weak aggregation and fail to strengthen intercellular adhesion over time, a process rescued by the expression of αE-catenin or chimeric E-cadherin·αE-catenins, including a chimera lacking the αE-catenin dimerization domain. Interestingly, an αE-catenin mutant lacking the modulation and actin-binding domains restores cadherin-dependent cell-cell contacts but cannot strengthen intercellular adhesion. The expression of αE-catenin mutated in its vinculin-binding site is defective in its ability to rescue cadherin-based adhesion strength in cells lacking αE-catenin. Vinculin depletion or the overexpression of the αE-catenin modulation domain strongly decreases E-cadherin-mediated adhesion strength. This supports the notion that both molecules are required for intercellular contact maturation. Furthermore, stretching of cell doublets increases vinculin recruitment and α18 anti-αE-catenin conformational epitope immunostaining at cell-cell contacts. Taken together, our results indicate that αE-catenin and vinculin cooperatively support intercellular adhesion strengthening, probably via a mechanoresponsive link between the E-cadherin·β-catenin complexes and the underlying actin cytoskeleton.
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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.