ArticleThe American journal of pathology2010
Plakoglobin rescues adhesive defects induced by ectodomain truncation of the desmosomal cadherin desmoglein 1: implications for exfoliative toxin-mediated skin blistering.
Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 38 citations in OpenAlex.
- Cadherin regulation of endoplasmic reticulum-plasma membrane contact sites.Cell reports · 2026Article
- Crosstalk in Skin: Loss of Desmoglein 1 in Keratinocytes Inhibits BRAFThe Journal of investigative dermatology · 2025Article
- Understanding host's response to staphylococcal scalded skin syndrome.Acta paediatrica (Oslo, Norway : 1992) · 2025Review
- ERK hyperactivation in epidermal keratinocytes impairs intercellular adhesion and drives Grover disease pathology.JCI insight · 2024Article
- Targeting SERCA2 in organotypic epidermis reveals MEK inhibition as a therapeutic strategy for Darier disease.JCI insight · 2023Article
- Commensal microbiota regulates skin barrier function and repair via signaling through the aryl hydrocarbon receptor.Cell host & microbe · 2021Article
- Damaged Keratin Filament Network Caused byFrontiers in genetics · 2021Article
- Desmoglein 1 Regulates Invadopodia by Suppressing EGFR/Erk Signaling in an Erbin-Dependent Manner.Molecular cancer research : MCR · 2019Article
- Nonmuscle myosin IIA is involved in recruitment of apical junction components through activation of α-catenin.Biology open · 2018Article
- Article
- Inflammation-induced desmoglein-2 ectodomain shedding compromises the mucosal barrier.Molecular biology of the cell · 2015Article
- A spontaneous deletion within the desmoglein 3 extracellular domain of mice results in hypomorphic protein expression, immunodeficiency, and a wasting disease phenotype.The American journal of pathology · 2015Article
- Plakophilin 3 mediates Rap1-dependent desmosome assembly and adherens junction maturation.Molecular biology of the cell · 2014Article
- Desmosomes: regulators of cellular signaling and adhesion in epidermal health and disease.Cold Spring Harbor perspectives in medicine · 2014Review
- The desmosomal protein desmoglein 1 aids recovery of epidermal differentiation after acute UV light exposure.The Journal of investigative dermatology · 2014Article
- Down-regulated γ-catenin expression is associated with tumor aggressiveness in esophageal cancer.World journal of gastroenterology · 2014Article
- Desmosome assembly and dynamics.Trends in cell biology · 2013Review
- Desmoglein-1/Erbin interaction suppresses ERK activation to support epidermal differentiation.The Journal of clinical investigation · 2013Article
- Cleavage of transmembrane junction proteins and their role in regulating epithelial homeostasis.Tissue barriers · 2013Review
- Differential downregulation of e-cadherin and desmoglein by epidermal growth factor.Dermatology research and practice · 2012Article
Corrections and comments
- Commented on by
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Desmoglein 1 (Dsg1) is a desmosomal cadherin that is essential to epidermal integrity. In the blistering diseases bullous impetigo and staphylococcal scalded-skin syndrome, pathogenesis depends on cleavage of Dsg1 by a bacterial protease, exfoliative toxin A, which removes residues 1 to 381 of the Dsg1 ectodomain. However, the cellular responses to Dsg1 cleavage that precipitate keratinocyte separation to induce blister formation are unknown. Here, we show that ectodomain-deleted Dsg1 (Δ381-Dsg1) mimics the toxin-cleaved cadherin, disrupts desmosomes, and reduces the mechanical integrity of keratinocyte sheets. In addition, we demonstrate that truncated Dsg1 remains associated with its catenin partner, plakoglobin, and causes a reduction in the levels of endogenous desmosomal cadherins in a dose-dependent manner, leading us to hypothesize that plakoglobin sequestration by truncated Dsg1 destabilizes other cadherins. Accordingly, a triple-point mutant of the ectodomain-deleted cadherin, which is uncoupled from plakoglobin, does not impair adhesion, indicating that this interaction is essential to the pathogenic potential of truncated Dsg1. Moreover, we demonstrate that increasing plakoglobin levels rescues cadherin expression, desmosome organization, and functional adhesion in cells expressing Δ381-Dsg1 or treated with exfoliative toxin A. Finally, we report that histone deacetylase inhibition up-regulates desmosomal cadherins and prevents the loss of adhesion induced by Dsg1 truncation. These findings further our understanding of the mechanism of exfoliative toxin-induced pathology and suggest novel strategies to suppress blistering in bulbous impetigo and staphylococcal scalded-skin syndrome.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.