ArticleiScience2025
Desmosomal cadherin tension loss in pemphigus vulgaris mediated by the inhibition of active RhoA at cell-cell adhesions.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Single Cell Mechanics in Disease Progression.Small science · 2026Review
- Protocol to quantify desmoglein 3 tension at cell-cell adhesions using FRET-based tension sensors.STAR protocols · 2026Article
- Desmoglein-driven dynamic signaling in pemphigus vulgaris: a systematic review of pathogenic pathways.NPJ Regenerative medicine · 2025Article
- Data-driven image analysis to determine antibody-induced dissociation of cell-cell adhesion and antibody pathogenicity in pemphigus.PNAS nexus · 2025Article
- Meeting report - Alpine desmosome disease meeting 2024: advances and emerging topics in desmosomes and related diseases.Journal of cell science · 2025Article
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Authors and funding
19 authors.
Funding
Abstract
Autoantibody binding to keratinocyte surface antigens, primarily desmoglein 3 (Dsg3) in the desmosome, leads to dissociation of cell-cell adhesions in pemphigus vulgaris. Much of the biophysical transformations after antibody binding remain underexplored. It is unclear how tensions in desmosomes and cell-cell adhesion structures change in response to antibodies, and how the altered tensional states translate to cellular responses. Here, using fluorescence resonance energy transfer-based tension sensors and traction force microscopy, we observed tension loss at Dsg3 and the entire cell-cell adhesion after antibody binding, along with potentially compensatory increase in junctional traction force at cell-extracellular matrix adhesions. Our data also indicate that this tension loss is mediated by RhoA inhibition at cell-cell contacts and can be partially restored by altering cell contractility. Collectively, these findings shed light on the biophysical mechanisms governing cell-cell interactions under autoimmune conditions, and may lead to therapies aimed at restoring tensional balance at cell-cell adhesions.
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Registered trials
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