ArticleThe Journal of investigative dermatology2015
Loss of Desmoglein Binding Is Not Sufficient for Keratinocyte Dissociation in Pemphigus.
Article in The Journal of investigative dermatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.
- What protein kinases are crucial for acantholysis and blister formation in pemphigus vulgaris? A systematic review.Journal of cellular physiology · 2022Pooled it
- Plakoglobin phosphorylation at serine 665 is capable of stabilizing cadherin-mediated adhesion in keratinocytes.JCI insight · 2026Article
- Desmoglein-driven dynamic signaling in pemphigus vulgaris: a systematic review of pathogenic pathways.NPJ Regenerative medicine · 2025Article
- Dsg3 epitope-specific signalling in pemphigus.Frontiers in immunology · 2023Article
- Desmoglein 2 can undergo CaBiophysical journal · 2022Article
- Mechanisms Causing Acantholysis in Pemphigus-Lessons from Human Skin.Frontiers in immunology · 2022Review
- Oxidative Stress-Mediated YAP Dysregulation Contributes to the Pathogenesis of Pemphigus Vulgaris.Frontiers in immunology · 2021Observational
- Autoantibody-Specific Signalling in Pemphigus.Frontiers in medicine · 2021Review
- The desmosome as a model for lipid raft driven membrane domain organization.Biochimica et biophysica acta. Biomembranes · 2020Review
- Scaling up single-cell mechanics to multicellular tissues - the role of the intermediate filament-desmosome network.Journal of cell science · 2020Review
- Dsg2 Upregulation as a Rescue Mechanism in Pemphigus.Frontiers in immunology · 2020Article
- Plakophilin 1 but not plakophilin 3 regulates desmoglein clustering.Cellular and molecular life sciences : CMLS · 2019Article
- Role of Src and Cortactin in Pemphigus Skin Blistering.Frontiers in immunology · 2019Article
- Role of Dsg1- and Dsg3-Mediated Signaling in Pemphigus Autoantibody-Induced Loss of Keratinocyte Cohesion.Frontiers in immunology · 2019Article
- Techniques to stimulate and interrogate cell-cell adhesion mechanics.Extreme Mechanics Letters · 2018Article
- Atomic Force Microscopy Provides New Mechanistic Insights into the Pathogenesis of Pemphigus.Frontiers in immunology · 2018Review
- Keratins Regulate p38MAPK-Dependent Desmoglein Binding Properties in Pemphigus.Frontiers in immunology · 2018Article
- Keratin Retraction and Desmoglein3 Internalization Independently Contribute to Autoantibody-Induced Cell Dissociation in Pemphigus Vulgaris.Frontiers in immunology · 2018Article
- Autoantibody Signaling in Pemphigus Vulgaris: Development of an Integrated Model.Frontiers in immunology · 2018Review
- Soluble Fas Ligand Is Essential for Blister Formation in Pemphigus.Frontiers in immunology · 2018Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pemphigus vulgaris (PV) is a severe autoimmune disease in which autoantibodies against the desmosomal cell adhesion molecules desmoglein (Dsg) 1 and Dsg3 cause intraepidermal blister formation. Mechanistically, the fundamental question is still unresolved whether loss of cell cohesion is a result of (1) direct inhibition of Dsg interaction by autoantibodies or (2) intracellular signaling events, which are altered in response to antibody binding and finally cause desmosome destabilization. We used atomic force microscopy (AFM) to perform Dsg3 adhesion measurements on living keratinocytes to investigate the contributions of direct inhibition and signaling to loss of cell cohesion after autoantibody treatment. Dsg3 binding was rapidly blocked following antibody exposure under conditions where no depletion of surface Dsg3 was detectable, demonstrating direct inhibition of Dsg3 interaction. Inhibition of p38MAPK, a central signaling molecule in PV pathogenesis, abrogated loss of cell cohesion, but had a minor effect on loss of Dsg3 binding. Similarly, the cholesterol-depleting agent methyl-β-cyclodextrin (β-MCD) fully blocked cell dissociation, but did not restore Dsg3 interactions or prevent the activation of p38MAPK. These results demonstrate that inhibition of Dsg3 binding is not sufficient to cause loss of cell cohesion, but rather alters signaling events which, in lipid raft-dependent manner, induce cell dissociation.
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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.