ArticleCell death & disease2019
The desmosomal cadherin desmoglein-3 acts as a keratinocyte anti-stress protein via suppression of p53.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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.
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Who cites it
20 citing papers in PubMed, 29 citations in OpenAlex.
- Targeting ST18-mediated pathomechanism in pemphigus vulgaris through voltage-dependent anion channel inhibition.Skin health and disease · 2026Article
- Circulating Antibodies Against DSG1 and DSG3 in Patients with Oral Lichen Planus: A Scoping Review.Antibodies (Basel, Switzerland) · 2025Review
- Differential Expression of Hard Tissue Proteins in Hypomineralized Second Primary Molars in Comparison to Normal Teeth.Clinical and experimental dental research · 2025Article
- Contribution of Keratinocytes in Skin Cancer Initiation and Progression.International journal of molecular sciences · 2024Review
- Mutant TP53 promotes invasion of lung cancer cells by regulating desmoglein 3.Journal of cancer research and clinical oncology · 2024Article
- Desmosomes at a glance.Journal of cell science · 2024Review
- ZNPs reduce epidermal mechanical strain resistance by promoting desmosomal cadherin endocytosis via mTORC1-TFEB-BLOC1S3 axis.Journal of nanobiotechnology · 2024Article
- Comparative Transcriptome Analysis Identifies Desmoglein-3 as a Potential Oncogene in Oral Cancer Cells.Cells · 2023Article
- YAP Inhibition by Verteporfin Causes Downregulation of Desmosomal Genes and Proteins Leading to the Disintegration of Intercellular Junctions.Life (Basel, Switzerland) · 2022Article
- Sacral Dimple, Conjunctiva, and Nipple as Less Obvious Pemphigus Vulgaris Locations around Natural Body Orifices: A Report of Three Cases.Journal of clinical medicine · 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-3 induces YAP phosphorylation and inactivation during collective migration of oral carcinoma cells.Molecular oncology · 2022Article
- Marked to Die-Cell Death Mechanisms for Keratinocyte Acantholysis in Pemphigus Diseases.Life (Basel, Switzerland) · 2022Review
- Desmosomal Cadherins in Health and Disease.Annual review of pathology · 2022Review
- Subtyping of Human Papillomavirus-Positive Cervical Cancers Based on the Expression Profiles of 50 Genes.Frontiers in immunology · 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
- The role of YAP in the control of the metastatic potential of oral cancer.Oncology research · 2021Review
- Oxidative Stress-Mediated YAP Dysregulation Contributes to the Pathogenesis of Pemphigus Vulgaris.Frontiers in immunology · 2021Observational
- Tracing the Evolutionary Origin of Desmosomes.Current biology : CB · 2020Review
- Desmosomes: Essential contributors to an integrated intercellular junction network.F1000Research · 2019Review
Corrections and comments
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Authors and funding
16 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Desmoglein-3 (Dsg3), the Pemphigus Vulgaris (PV) antigen (PVA), plays an essential role in keratinocyte cell-cell adhesion and regulates various signaling pathways involved in the progression and metastasis of cancer where it is upregulated. We show here that expression of Dsg3 impacts on the expression and function of p53, a key transcription factor governing the responses to cellular stress. Dsg3 depletion increased p53 expression and activity, an effect enhanced by treating cells with UVB, mechanical stress and genotoxic drugs, whilst increased Dsg3 expression resulted in the opposite effects. Such a pathway in the negative regulation of p53 by Dsg3 was Dsg3 specific since neither E-cadherin nor desmoplakin knockdown caused similar effects. Analysis of Dsg3
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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.