ArticleFrontiers in immunology2018
Keratins Regulate p38MAPK-Dependent Desmoglein Binding Properties in Pemphigus.
Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 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
- Data-driven image analysis to determine antibody-induced dissociation of cell-cell adhesion and antibody pathogenicity in pemphigus.PNAS nexus · 2025Article
- Epac1 contributes to apremilast-mediated rescue of pemphigus autoantibody-induced loss of keratinocyte adhesion.JCI insight · 2025Article
- shRNA-Targeting Caspase-3 Inhibits Cell Detachment Induced by Pemphigus Vulgaris Autoantibodies inInternational journal of molecular sciences · 2024Article
- Catalytic antibodies in arrhythmogenic cardiomyopathy patients cleave desmoglein 2 and N-cadherin and impair cardiomyocyte cohesion.Cellular and molecular life sciences : CMLS · 2023Article
- Dsg3 epitope-specific signalling in pemphigus.Frontiers in immunology · 2023Article
- Identification of Six microRNAs as Potential Biomarkers for Pemphigus Vulgaris: From Diagnosis to Pathogenesis.Diagnostics (Basel, Switzerland) · 2022Article
- Up-regulation of ST18 in pemphigus vulgaris drives a self-amplifying p53-dependent pathomechanism resulting in decreased desmoglein 3 expression.Scientific reports · 2022Article
- Desmoglein 2 can undergo CaBiophysical journal · 2022Article
- Bidirectional regulation of desmosome hyperadhesion by keratin isotypes and desmosomal components.Cellular and molecular life sciences : CMLS · 2022Article
- Pemphigus Foliaceus Autoantibodies Induce Redistribution Primarily of Extradesmosomal Desmoglein 1 in the Cell Membrane.Frontiers in immunology · 2022Article
- Autoantibody-Specific Signalling in Pemphigus.Frontiers in medicine · 2021Review
- Desmosomal Hyperadhesion Is Accompanied with Enhanced Binding Strength of Desmoglein 3 Molecules.Biophysical journal · 2020Article
- Cardiomyocyte adhesion and hyperadhesion differentially require ERK1/2 and plakoglobin.JCI insight · 2020Article
- Plakophilin 1 but not plakophilin 3 regulates desmoglein clustering.Cellular and molecular life sciences : CMLS · 2019Article
- Role of Dsg1- and Dsg3-Mediated Signaling in Pemphigus Autoantibody-Induced Loss of Keratinocyte Cohesion.Frontiers in immunology · 2019Article
- ST18 Enhances PV-IgG-Induced Loss of Keratinocyte Cohesion in Parallel to Increased ERK Activation.Frontiers in immunology · 2019Article
- Atomic Force Microscopy Provides New Mechanistic Insights into the Pathogenesis of Pemphigus.Frontiers in immunology · 2018Review
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Keratins are crucial for the anchorage of desmosomes. Severe alterations of keratin organization and detachment of filaments from the desmosomal plaque occur in the autoimmune dermatoses pemphigus vulgaris and pemphigus foliaceus (PF), which are mainly caused by autoantibodies against desmoglein (Dsg) 1 and 3. Keratin alterations are a structural hallmark in pemphigus pathogenesis and correlate with loss of intercellular adhesion. However, the significance for autoantibody-induced loss of intercellular adhesion is largely unknown. In wild-type (wt) murine keratinocytes, pemphigus autoantibodies induced keratin filament retraction. Under the same conditions, we used murine keratinocytes lacking all keratin filaments (KtyII k.o.) as a model system to dissect the role of keratins in pemphigus. KtyII k.o. cells show compromised intercellular adhesion without antibody (Ab) treatment, which was not impaired further by pathogenic pemphigus autoantibodies. Nevertheless, direct activation of p38MAPK
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