ReviewAnnals of dermatology2015
Recently Identified Forms of Epidermolysis Bullosa.
Review in Annals of dermatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed.
- Article
- Development of pathological skin models: from conventional techniques to 3D bioprinting.Frontiers in bioengineering and biotechnology · 2025Review
- Parents' perception of challenges of caring of children with Epidermolysis bullosa: a qualitative study.BMC research notes · 2024Article
- Skin Development and Disease: A Molecular Perspective.Current issues in molecular biology · 2024Review
- Roles of dystonin isoforms in the maintenance of neural, muscle, and cutaneous tissues.Anatomical science international · 2024Review
- Stem Cell Therapies for Epidermolysis Bullosa Treatment.Bioengineering (Basel, Switzerland) · 2023Review
- Epidermolysis Bullosa-A Different Genetic Approach in Correlation with Genetic Heterogeneity.Diagnostics (Basel, Switzerland) · 2022Review
- Bioengineered Efficacy Models of Skin Disease: Advances in the Last 10 Years.Pharmaceutics · 2022Review
- Keratins as an Inflammation Trigger Point in Epidermolysis Bullosa Simplex.International journal of molecular sciences · 2021Review
- Pathogenetic Therapy of Epidermolysis Bullosa: Current State and Prospects.Bulletin of experimental biology and medicine · 2021Review
- Mucopolysaccharidosis III: Molecular basis and treatment.Pediatric endocrinology, diabetes, and metabolism · 2021Review
- The Tongue Squamous Carcinoma Cell Line Cal27 Primarily Employs Integrin α6β4-Containing Type II Hemidesmosomes for Adhesion Which Contribute to Anticancer Drug Sensitivity.Frontiers in cell and developmental biology · 2021Article
- The Human Epidermal Basement Membrane: A Shaped and Cell Instructive Platform That Aging Slowly Alters.Biomolecules · 2020Review
- Apparent Missense Variant in COL7A1 Causes a Severe Form of Recessive Dystrophic Epidermolysis Bullosa via Effects on Splicing.Acta dermato-venereologica · 2020Article
- Diverse dystonin gene mutations cause distinct patterns ofDisease models & mechanisms · 2020Article
- Clinical practice guidelines for laboratory diagnosis of epidermolysis bullosa.The British journal of dermatology · 2020Article
- Genetic Base of Behavioral Disorders in Mucopolysaccharidoses: Transcriptomic Studies.International journal of molecular sciences · 2020Article
- Hemidesmosomes modulate force generation via focal adhesions.The Journal of cell biology · 2020Article
- Recent Advances and Prospects in the Research of Nascent Adhesions.Frontiers in physiology · 2020Review
- A rare case of skin blistering and esophageal stenosis in the course of epidermolysis bullosa - case report and literature review.BMC gastroenterology · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epidermolysis bullosa (EB) comprises a collection of clinically diverse inherited blistering diseases that affect the skin and, in some subtypes, mucous membranes and other organs. Currently classified into four main subtypes (EB simplex, junctional EB, dystrophic EB, and Kindler syndrome, mainly based on the level of skin cleavage), the spectrum of EB extends to more than 30 clinical subtypes with pathogenic mutations in at least 18 distinct genes. This review focuses on three recent additions to variants of EB: all are autosomal recessive, and result from mutations in either DST-e (coding for epidermal dystonin, also known as the 230 kDa bullous pemphigoid antigen, BP230), EXPH5 (coding for exophilin-5, also known as Slac2-b), or ITGA3 (coding for the integrin alpha-3 subunit). Each of these new forms of EB is reviewed with respect to the initial gene discovery, clinical features, the current mutation database, and skin pathology. Awareness of these recently described forms of EB is helpful in the clinical evaluation of patients with EB and in defining genotype-phenotype correlation for inherited blistering skin diseases.
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.