ArticleThe Journal of allergy and clinical immunology2019
EMSY expression affects multiple components of the skin barrier with relevance to atopic dermatitis.
Article in The Journal of allergy and clinical immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 papers, 1 of them a synthesis that pooled it.
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
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
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- Replication and meta-analyses nominate numerous eosinophilic esophagitis risk genes.The Journal of allergy and clinical immunology · 2021Pooled it
- Genome-Wide Cross-Trait Analysis in European Populations Reveals Shared Genetic Architecture of Chronic Obstructive Pulmonary Disease and the Allergy Spectrum.International archives of allergy and immunology · 2025Article
- Review
- Genome-wide identification of dysregulated alternative splicing and RNA-binding proteins involved in atopic dermatitis.Frontiers in genetics · 2024Article
- Prenatal Maternal Risk Factors Contributing to Atopic Dermatitis: A Systematic Review and Meta-Analysis of Cohort Studies.Annals of dermatology · 2023Article
- pTINCR microprotein promotes epithelial differentiation and suppresses tumor growth through CDC42 SUMOylation and activation.Nature communications · 2022Article
- Article
- Break on through: The role of innate immunity and barrier defence in atopic dermatitis and psoriasis.Skin health and disease · 2022Review
- Genetic/Environmental Contributions and Immune Dysregulation in Children with Atopic Dermatitis.Journal of asthma and allergy · 2022Review
- Update on the Pathogenesis and Therapy of Atopic Dermatitis.Clinical reviews in allergy & immunology · 2021Review
- Triangulating Molecular Evidence to Prioritize Candidate Causal Genes at Established Atopic Dermatitis Loci.The Journal of investigative dermatology · 2021Article
- Recent advances in atopic dermatitis.Current opinion in immunology · 2020Review
- Genetics in Atopic Dermatitis: Historical Perspective and Future Prospects.Acta dermato-venereologica · 2020Review
- Functional and proteomic analysis of a full thickness filaggrin-deficient skin organoid model.Wellcome open research · 2019Article
Corrections and comments
- Erratum issuedCorrigenda.2020
Authors and funding
17 authors at 5 institutions in 1 country.
Funding
Abstract
backgroundAtopic dermatitis (AD) is a common, complex, and highly heritable inflammatory skin disease. Genome-wide association studies offer opportunities to identify molecular targets for drug development. A risk locus on chromosome 11q13.5 lies between 2 candidate genes, EMSY and LRRC32 (leucine-rich repeat-containing 32) but the functional mechanisms affecting risk of AD remain unclear.
objectivesWe sought to apply a combination of genomic and molecular analytic techniques to investigate which genes are responsible for genetic risk at this locus and to define mechanisms contributing to atopic skin disease.
methodsWe used interrogation of available genomic and chromosome conformation data in keratinocytes, small interfering RNA (siRNA)-mediated knockdown in skin organotypic culture and functional assessment of barrier parameters, mass spectrometric global proteomic analysis and quantitative lipid analysis, electron microscopy of organotypic skin, and immunohistochemistry of human skin samples.
resultsGenomic data indicate active promoters in the genome-wide association study locus and upstream of EMSY; EMSY, LRRC32, and intergenic variants all appear to be within a single topologically associating domain. siRNA-knockdown of EMSY in organotypic culture leads to enhanced development of barrier function, reflecting increased expression of structural and functional proteins, including filaggrin and filaggrin-2, as well as long-chain ceramides. Conversely, overexpression of EMSY in keratinocytes leads to a reduction in markers of barrier formation. Skin biopsy samples from patients with AD show greater EMSY staining in the nucleus, which is consistent with an increased functional effect of this transcriptional control protein.
conclusionOur findings demonstrate an important role for EMSY in transcriptional regulation and skin barrier formation, supporting EMSY inhibition as a therapeutic approach.
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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.