ArticleBiophysical journal2021
Computational model of E-cadherin clustering under force.
Article in Biophysical journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- Structural Insights into Ordered Multicomponent Assemblies in Cell Junctions.Advances in experimental medicine and biology · 2026Review
- Paths to stability - actin regulation of adherens junction mechanics.Journal of cell science · 2025Review
- Observation of E-cadherin adherens junction dynamics with metal-induced energy transfer imaging and spectroscopy.Communications biology · 2024Article
- Insights gained from computational modeling of YAP/TAZ signaling for cellular mechanotransduction.NPJ systems biology and applications · 2024Review
- A computational study for understanding the impact of p120-catenin on the cis-dimerization of cadherin.Journal of molecular cell biology · 2024Article
- Dynamics and functions of E-cadherin complexes in epithelial cell and tissue morphogenesis.Marine life science & technology · 2023Review
- Mechanics of cell-cell junctions.Biophysical journal · 2023Article
- A multi-material platform for imaging of single cell-cell junctions under tensile load fabricated with two-photon polymerization.Biomedical microdevices · 2022Article
- Intrinsic cell rheology drives junction maturation.Nature communications · 2022Article
- Powering morphogenesis: multiscale challenges at the interface of cell adhesion and the cytoskeleton.Molecular biology of the cell · 2022Review
- Role of actin filaments and cis binding in cadherin clustering and patterning.PLoS computational biology · 2022Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
E-cadherins play a critical role in the formation of cell-cell adhesions for several physiological functions, including tissue development, repair, and homeostasis. The formation of clusters of E-cadherins involves extracellular adhesive (trans-) and lateral (cis-) associations between E-cadherin ectodomains and stabilization through intracellular binding to the actomyosin cytoskeleton. This binding provides force to the adhesion and is required for mechanotransduction. However, the exact role of cytoskeletal force on the clustering of E-cadherins is not well understood. To gain insights into this mechanism, we developed a computational model based on Brownian dynamics. In the model, E-cadherins transit between structural and functional states; they are able to bind and unbind other E-cadherins on the same and/or opposite cell(s) through trans- and cis-interactions while also creating dynamic links with the actomyosin cytoskeleton. Our results show that actomyosin force governs the fraction of E-cadherins in clusters and the size and number of clusters. For low forces (below 10 pN), a large number of small E-cadherin clusters form with less than five E-cadherins each. At higher forces, the probability of forming fewer but larger clusters increases. These findings support the idea that force reinforces cell-cell adhesions, which is consistent with differences in cluster size previously observed between apical and lateral junctions of epithelial tissues.
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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.