ArticlePLoS genetics2016
Identification of a Functional Risk Variant for Pemphigus Vulgaris in the ST18 Gene.
Article in PLoS genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 50 citations in OpenAlex.
- Targeting ST18-mediated pathomechanism in pemphigus vulgaris through voltage-dependent anion channel inhibition.Skin health and disease · 2026Article
- Genetic variations in theDermatology reports · 2025Article
- Autoimmune pemphigus: difficulties in diagnosis and the molecular mechanisms underlying the disease.Frontiers in immunology · 2025Review
- Association of Human Endogenous Retrovirus-W (HERV-W) Copies with Pemphigus Vulgaris.Current molecular medicine · 2024Article
- AssessingJournal of medicine and life · 2024Article
- Coexistence of malignancies in pemphigus vulgaris.Immunologic research · 2023Article
- Detection of herpes simplex viruses in the oral lesions of patients with pemphigus vulgaris: Is it diagnostic or predictive of disease severity?Skin health and disease · 2023Article
- Pemphigus: trigger and predisposing factors.Frontiers in medicine · 2023Review
- Up-regulation of ST18 in pemphigus vulgaris drives a self-amplifying p53-dependent pathomechanism resulting in decreased desmoglein 3 expression.Scientific reports · 2022Article
- Autoimmune Pemphigus: Latest Advances and Emerging Therapies.Frontiers in molecular biosciences · 2021Review
- Beyond the HLA polymorphism: A complex pattern of genetic susceptibility to pemphigus.Genetics and molecular biology · 2020Article
- The pathogenesis of bullous skin diseases.Journal of translational autoimmunity · 2019Review
- Expression of human endogenous retroviruses in pemphigus vulgaris patients.Molecular biology reports · 2019Article
- ST18 Enhances PV-IgG-Induced Loss of Keratinocyte Cohesion in Parallel to Increased ERK Activation.Frontiers in immunology · 2019Article
- Skin Barrier and Autoimmunity-Mechanisms and Novel Therapeutic Approaches for Autoimmune Blistering Diseases of the Skin.Frontiers in immunology · 2019Review
- Pemphigus: Current and Future Therapeutic Strategies.Frontiers in immunology · 2019Review
- Tyrosine Kinases in Autoimmune and Inflammatory Skin Diseases.Frontiers in immunology · 2019Review
- Filaggrin 2 Deficiency Results in Abnormal Cell-Cell Adhesion in the Cornified Cell Layers and Causes Peeling Skin Syndrome Type A.The Journal of investigative dermatology · 2018Article
- The Genetics of Pemphigus Vulgaris.Frontiers in medicine · 2018Review
- Non-Desmoglein Antibodies in Patients With Pemphigus Vulgaris.Frontiers in immunology · 2018Review
Corrections and comments
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Authors and funding
17 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pemphigus vulgaris (PV) is a life-threatening autoimmune mucocutaneous blistering disease caused by disruption of intercellular adhesion due to auto-antibodies directed against epithelial components. Treatment is limited to immunosuppressive agents, which are associated with serious adverse effects. The propensity to develop the disease is in part genetically determined. We therefore reasoned that the delineation of PV genetic basis may point to novel therapeutic strategies. Using a genome-wide association approach, we recently found that genetic variants in the vicinity of the ST18 gene confer a significant risk for the disease. Here, using targeted deep sequencing, we identified a PV-associated variant residing within the ST18 promoter region (p<0.0002; odds ratio = 2.03). This variant was found to drive increased gene transcription in a p53/p63-dependent manner, which may explain the fact that ST18 is up-regulated in the skin of PV patients. We then discovered that when overexpressed, ST18 stimulates PV serum-induced secretion of key inflammatory molecules and contributes to PV serum-induced disruption of keratinocyte cell-cell adhesion, two processes previously implicated in the pathogenesis of PV. Thus, the present findings indicate that ST18 may play a direct role in PV and consequently represents a potential target for the treatment of this disease.
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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.