ArticleThe Journal of cell biology2001
A central role for the armadillo protein plakoglobin in the autoimmune disease pemphigus vulgaris.
Article in The Journal of cell biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 189 citations in OpenAlex.
- Desmoglein-driven dynamic signaling in pemphigus vulgaris: a systematic review of pathogenic pathways.NPJ Regenerative medicine · 2025Article
- shRNA-Targeting Caspase-3 Inhibits Cell Detachment Induced by Pemphigus Vulgaris Autoantibodies inInternational journal of molecular sciences · 2024Article
- A desmosomal cadherin controls multipotent hair follicle stem cell quiescence and orchestrates regeneration through adhesion signaling.iScience · 2023Article
- The intercalated disc: a unique organelle for electromechanical synchrony in cardiomyocytes.Physiological reviews · 2023Review
- Significance of anti-desmocollin autoantibodies in pemphigus.The Journal of dermatology · 2023Review
- In Vitro, Ex Vivo, and In Vivo Models for the Study of Pemphigus.International journal of molecular sciences · 2022Review
- Apoptolysis: a less understood concept in the pathogenesis of Pemphigus Vulgaris.Apoptosis : an international journal on programmed cell death · 2022Review
- Pitfalls in the Application of Dispase-Based Keratinocyte Dissociation Assay for In Vitro Analysis of Pemphigus Vulgaris.Vaccines · 2022Article
- Innate immune activation as cofactor in pemphigus disease manifestation.Frontiers in immunology · 2022Article
- Immunotherapy for Pemphigus: Present and Future.Frontiers in medicine · 2022Review
- 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 pathogenesis of bullous skin diseases.Journal of translational autoimmunity · 2019Review
- Pemphigus: a Comprehensive Review on Pathogenesis, Clinical Presentation and Novel Therapeutic Approaches.Clinical reviews in allergy & immunology · 2018Review
- Non-Desmoglein Antibodies in Patients With Pemphigus Vulgaris.Frontiers in immunology · 2018Review
- Autoantibody Signaling in Pemphigus Vulgaris: Development of an Integrated Model.Frontiers in immunology · 2018Review
- Keratins Regulate p38MAPK-Dependent Desmoglein Binding Properties in Pemphigus.Frontiers in immunology · 2018Article
- Mechanisms of Autoantibody-Induced Pathology.Frontiers in immunology · 2017Review
- Mechanisms of Disease: Pemphigus and Bullous Pemphigoid.Annual review of pathology · 2016Review
4 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In pemphigus vulgaris (PV), autoantibody binding to desmoglein (Dsg) 3 induces loss of intercellular adhesion in skin and mucous membranes. Two hypotheses are currently favored to explain the underlying molecular mechanisms: (a) disruption of adhesion through steric hindrance, and (b) interference of desmosomal cadherin-bound antibody with intracellular events, which we speculated to involve plakoglobin. To investigate the second hypothesis we established keratinocyte cultures from plakoglobin knockout (PG-/-) embryos and PG+/+ control mice. Although both cell types exhibited desmosomal cadherin-mediated adhesion during calcium-induced differentiation and bound PV immunoglobin (IgG) at their cell surface, only PG+/+ keratinocytes responded with keratin retraction and loss of adhesion. When full-length plakoglobin was reintroduced into PG-/- cells, responsiveness to PV IgG was restored. Moreover, in these cells like in PG+/+ keratinocytes, PV IgG binding severely affected the linear distribution of plakoglobin at the plasma membrane. Taken together, the establishment of an in vitro model using PG+/+ and PG-/- keratinocytes allowed us (a) to exclude the steric hindrance only hypothesis, and (b) to demonstrate for the first time that plakoglobin plays a central role in PV, a finding that will provide a novel direction for investigations of the molecular mechanisms leading to PV, and on the function of plakoglobin in differentiating keratinocytes.
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