ArticleThe Journal of biological chemistry2009
Peptides Targeting the Desmoglein 3 Adhesive Interface Prevent Autoantibody-induced Acantholysis in Pemphigus.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 38 citations in OpenAlex.
- Desmoglein-driven dynamic signaling in pemphigus vulgaris: a systematic review of pathogenic pathways.NPJ Regenerative medicine · 2025Article
- Desmoglein 2 can undergo CaBiophysical journal · 2022Article
- Desmoglein2 Regulates Claudin2 Expression by Sequestering PI-3-Kinase in Intestinal Epithelial Cells.Frontiers in immunology · 2021Article
- Autoantibody-Specific Signalling in Pemphigus.Frontiers in medicine · 2021Review
- Identification of novel therapeutic targets for blocking acantholysis in pemphigus.British journal of pharmacology · 2020Article
- [Therapy of pemphigus].Der Hautarzt; Zeitschrift fur Dermatologie, Venerologie, und verwandte Gebiete · 2019Review
- Keratins Regulate p38MAPK-Dependent Desmoglein Binding Properties in Pemphigus.Frontiers in immunology · 2018Article
- Pemphigus-A Disease of Desmosome Dysfunction Caused by Multiple Mechanisms.Frontiers in immunology · 2018Review
- Atomic Force Microscopy Provides New Mechanistic Insights into the Pathogenesis of Pemphigus.Frontiers in immunology · 2018Review
- Setting the target for pemphigus vulgaris therapy.JCI insight · 2017Review
- Desmoglein 2 compensates for desmoglein 3 but does not control cell adhesion via regulation of p38 mitogen-activated protein kinase in keratinocytes.The Journal of biological chemistry · 2014Article
- Peptide-mediated desmoglein 3 crosslinking prevents pemphigus vulgaris autoantibody-induced skin blistering.The Journal of clinical investigation · 2013Article
- Article
- In vitro functional analyses of arrhythmogenic right ventricular cardiomyopathy-associated desmoglein-2-missense variations.PloS one · 2012Article
- Experimental human cell and tissue models of pemphigus.Dermatology research and practice · 2010Article
- Desmocollin 3-mediated binding is crucial for keratinocyte cohesion and is impaired in pemphigus.The Journal of biological chemistry · 2009Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pemphigus vulgaris (PV) autoantibodies directly inhibit desmoglein (Dsg) 3-mediated transinteraction. Because cellular signaling also seems to be required for PV pathogenesis, it is important to characterize the role of direct inhibition in pemphigus acantholysis to allow establishment of new therapeutic approaches. Therefore, we modeled the Dsg1 and Dsg3 sequences into resolved cadherin structures and predicted peptides targeting the adhesive interface of both Dsg3 and Dsg1. In atomic force microscopy single molecule experiments, the self-designed cyclic single peptide specifically blocked homophilic Dsg3 and Dsg1 transinteraction, whereas a tandem peptide (TP) consisting of two combined single peptides did not. TP did not directly block binding of pemphigus IgG to their target Dsg antigens but prevented PV-IgG-induced inhibition of Dsg3 transinteraction in cell-free (atomic force microscopy) and cell-based (laser tweezer) experiments, indicating stabilization of Dsg3 bonds. Similarly, PV-IgG-mediated acantholysis and disruption of Dsg3 localization in HaCaT keratinocytes was partially blocked by TP. This is the first evidence that direct inhibition of Dsg3 binding is important for PV pathogenesis and that peptidomimetics stabilizing Dsg transinteraction may provide a novel approach for PV treatment.
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