ArticleBiology open2015
There are four dynamically and functionally distinct populations of E-cadherin in cell junctions.
Article in Biology open, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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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.
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Who cites it
13 citing papers in PubMed, 51 citations in OpenAlex.
- A key role of Canoe's intrinsically disordered region in linking cell junctions to the cytoskeleton.The Journal of cell biology · 2025Article
- The Scribble/SGEF/Dlg1 complex regulates the stability of apical junctions in epithelial cells.bioRxiv : the preprint server for biology · 2024Article
- Powering morphogenesis: multiscale challenges at the interface of cell adhesion and the cytoskeleton.Molecular biology of the cell · 2022Review
- Computational model of E-cadherin clustering under force.Biophysical journal · 2021Article
- Actin-based force generation and cell adhesion in tissue morphogenesis.Current biology : CB · 2021Review
- Celsr1 adhesive interactions mediate the asymmetric organization of planar polarity complexes.eLife · 2021Article
- Interactions and Feedbacks in E-Cadherin Transcriptional Regulation.Frontiers in cell and developmental biology · 2021Article
- Arf6 determines tissue architecture by stabilizing intercellular adhesion.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2020Article
- Cadherin clusters stabilized by a combination of specific and nonspecific cis-interactions.eLife · 2020Article
- Spatial and temporal organization of cadherin in punctate adherens junctions.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- WAVE regulates Cadherin junction assembly and turnover during epithelial polarization.Developmental biology · 2018Article
- Formin-mediated actin polymerization at cell-cell junctions stabilizes E-cadherin and maintains monolayer integrity during wound repair.Molecular biology of the cell · 2016Article
- Focusing super resolution on the cytoskeleton.F1000Research · 2016Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
E-cadherin is a trans-membrane tumor suppressor responsible for epithelial cell adhesion. E-cadherin forms adhesive clusters through combined extra-cellular cis- and trans-interactions and intracellular interaction with the actin cytoskeleton. Here we identify four populations of E-cadherin within cell junctions based on the molecular interactions which determine their mobility and adhesive properties. Adhesive and non-adhesive populations of E-cadherin each consist of mobile and immobile fractions. Up to half of the E-cadherin immobilized in cell junctions is non-adhesive. Incorporation of E-cadherin into functional adhesions require all three adhesive interactions, with deletion of any one resulting in loss of effective cell-cell adhesion. Interestingly, the only interaction which could independently slow the diffusion of E-cadherin was the tail-mediated intra-cellular interaction. The adhesive and non-adhesive mobile fractions of E-cadherin can be distinguished by their sensitivity to chemical cross-linking with adhesive clusters. Our data define the size, mobility, and adhesive properties of four distinct populations of E-cadherin within cell junctions, and support association with the actin cytoskeleton as the first step in adhesion formation.
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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.