ArticlePloS one2010
Desmoglein 3, via an interaction with E-cadherin, is associated with activation of Src.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
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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
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Who cites it
36 citing papers in PubMed, 61 citations in OpenAlex.
- Proteome and miRNAs Expression in Medication-Related Osteonecrosis of the Jaw.International journal of molecular sciences · 2026Article
- Desmosomal cadherin tension loss in pemphigus vulgaris mediated by the inhibition of active RhoA at cell-cell adhesions.iScience · 2025Article
- DSG3 promotes bladder cancer growth and metastasis via AKT/GSK3β/β-catenin pathway.Journal of translational medicine · 2025Article
- Desmosomal Cadherin Tension Loss in Pemphigus Vulgaris Mediated by the Inhibition of Active RhoA at Cell-Cell Adhesions.bioRxiv : the preprint server for biology · 2024Article
- Proximity Mapping of Desmosomes Reveals a Striking Shift in Their Molecular Neighborhood Associated With Maturation.Molecular & cellular proteomics : MCP · 2024Article
- Comparative Transcriptome Analysis Identifies Desmoglein-3 as a Potential Oncogene in Oral Cancer Cells.Cells · 2023Article
- Dsg3 epitope-specific signalling in pemphigus.Frontiers in immunology · 2023Article
- The Regulation of the Hippo Pathway by Intercellular Junction Proteins.Life (Basel, Switzerland) · 2022Review
- YAP Inhibition by Verteporfin Causes Downregulation of Desmosomal Genes and Proteins Leading to the Disintegration of Intercellular Junctions.Life (Basel, Switzerland) · 2022Article
- Article
- Desmoglein 2 can undergo CaBiophysical journal · 2022Article
- Desmoglein-3 induces YAP phosphorylation and inactivation during collective migration of oral carcinoma cells.Molecular oncology · 2022Article
- Characterization of Desmoglein 3 (DSG3) as a Sensitive and Specific Marker for Esophageal Squamous Cell Carcinoma.Gastroenterology research and practice · 2022Article
- Evolving Mechanisms in the Pathophysiology of Pemphigus Vulgaris: A Review Emphasizing the Role of Desmoglein 3 in Regulating p53 and the Yes-Associated Protein.Life (Basel, Switzerland) · 2021Review
- Desmoglein-2 harnesses a PDZ-GEF2/Rap1 signaling axis to control cell spreading and focal adhesions independent of cell-cell adhesion.Scientific reports · 2021Article
- Desmoglein 3 contributes to tumorigenicity of pancreatic ductal adenocarcinoma through activating Src-FAK signaling.Animal cells and systems · 2021Article
- Oxidative Stress-Mediated YAP Dysregulation Contributes to the Pathogenesis of Pemphigus Vulgaris.Frontiers in immunology · 2021Observational
- Evidence for the Desmosomal Cadherin Desmoglein-3 in Regulating YAP and Phospho-YAP in Keratinocyte Responses to Mechanical Forces.International journal of molecular sciences · 2019Article
- The desmosomal cadherin desmoglein-3 acts as a keratinocyte anti-stress protein via suppression of p53.Cell death & disease · 2019Article
- Role of Src and Cortactin in Pemphigus Skin Blistering.Frontiers in immunology · 2019Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundDesmoglein 3 (Dsg3), a desmosomal adhesion protein, is expressed in basal and immediate suprabasal layers of skin and across the entire stratified squamous epithelium of oral mucosa. However, increasing evidence suggests that the role of Dsg3 may involve more than just cell-cell adhesion. METHODOLOGY/PRINCIPAL
findingsTo determine possible additional roles of Dsg3 during epithelial cell adhesion we used overexpression of full-length human Dsg3 cDNA, and RNAi-mediated knockdown of this molecule in various epithelial cell types. Overexpression of Dsg3 resulted in a reduced level of E-cadherin but a colocalisation with the E-cadherin-catenin complex of the adherens junctions. Concomitantly these transfected cells exhibited marked migratory capacity and the formation of filopodial protrusions. These latter events are consistent with Src activation and, indeed, Src-specific inhibition reversed these phenotypes. Moreover Dsg3 knockdown, which also reversed the decreased level of E-cadherin, partially blocked Src phosphorylation. CONCLUSIONS/SIGNIFICANCE: Our data are consistent with the possibility that Dsg3, as an up-stream regulator of Src activity, helps regulate adherens junction formation.
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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.