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Bead Aggregation Assays for the Characterization of Putative Cell Adhesion Molecules
Published on: October 17, 2014
E-cadherin dynamics is regulated by galectin-7 at epithelial cell surface.
Tamara Advedissian1, Véronique Proux-Gillardeaux1,2, Rachel Nkosi1
1Team Morphogenesis, Homeostasis and Pathologies, University Paris Diderot, Sorbonne Paris Cité, CNRS UMR 7592, Institut Jacques Monod, 15 Rue Hélène Brion, 75013, Paris, France.
Galectin-7 stabilizes E-cadherin at the cell membrane, enhancing keratinocyte collective migration and wound healing. This protein is crucial for maintaining cell adhesion and coordinated movement during epidermal repair.
Area of Science:
- Cell Biology
- Dermatology
- Biochemistry
Background:
- Epidermal wound re-epithelialization relies on keratinocyte collective cell migration.
- Intercellular adhesion, particularly adherens junctions, is vital for keratinocyte communication, tension, and coordinated movement.
- Galectin-7, a lectin in stratified epithelia, is known to influence cell migration and adhesion.
Purpose of the Study:
- To investigate the novel function of galectin-7 in regulating keratinocyte collective migration directionality and behavior.
- To identify galectin-7's role in the mechanisms governing adherens junctions and cell adhesion.
Main Methods:
- Investigated galectin-7's interaction with E-cadherin, a key adherens junction protein.
- Assessed the impact of galectin-7 on E-cadherin localization and endocytosis.
- Analyzed the effect of galectin-7 silencing on E-cadherin-mediated intercellular adhesion.
Main Results:
- Galectin-7 directly interacts with E-cadherin independently of glycosylation motifs.
- Galectin-7 stabilizes E-cadherin at the plasma membrane by inhibiting its endocytosis.
- Silencing galectin-7 reduces E-cadherin-mediated intercellular adhesion and affects collective cell migration.
Conclusions:
- Galectin-7 acts as a novel stabilizer of adherens junctions by modulating E-cadherin turnover.
- The interplay between E-cadherin dynamics and intercellular adhesion strength is critical for keratinocyte collective migration and wound healing.
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