ArticleThe Journal of biological chemistry2011
Epigenetic regulation of the IL-13-induced human eotaxin-3 gene by CREB-binding protein-mediated histone 3 acetylation.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
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.
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Who cites it
28 citing papers in PubMed, 51 citations in OpenAlex.
- Twin and family studies reveal strong environmental and weaker genetic cues explaining heritability of eosinophilic esophagitis.The Journal of allergy and clinical immunology · 2014Trial
- Review
- Emerging Insights into the Inflammatory Phenotypes of Eosinophilic Esophagitis.Journal of inflammation research · 2026Review
- From allergens to epigenetics: how histone acetylation shapes immune gene expression in allergic diseases.Epigenomics · 2025Review
- Genetic Background of Eosinophilic Esophagitis and Esophageal Atresia in Children.Digestive diseases and sciences · 2025Article
- Eosinophilic Esophagitis: The Role of Steroids and the Dose, Duration, and Delivery of Steroid Therapy.Cureus · 2024Review
- Molecular Mechanisms of Eosinophilic Esophagitis.International journal of molecular sciences · 2021Review
- Type 2 Inflammation in Eosinophilic Esophagitis: From Pathophysiology to Therapeutic Targets.Frontiers in physiology · 2021Review
- Challenges and updates in the management of eosinophilic esophagitis.Przeglad gastroenterologiczny · 2020Review
- Genetic, Inflammatory, and Epithelial Cell Differentiation Factors Control Expression of Human Calpain-14.G3 (Bethesda, Md.) · 2019Article
- Pathophysiology of Eosinophilic Esophagitis.Gastroenterology · 2018Review
- Genetics of eosinophilic esophagitis.Mucosal immunology · 2017Review
- IL-13 regulates human nasal epithelial cell differentiation via H3K4me3 modification.Journal of inflammation research · 2017Article
- IL-4 impairs wound healing potential in the skin by repressing fibronectin expression.The Journal of allergy and clinical immunology · 2017Article
- Mechanisms of Disease of Eosinophilic Esophagitis.Annual review of pathology · 2016Review
- Eosinophilic Esophagitis: A Comprehensive Review.Clinical reviews in allergy & immunology · 2016Review
- The Immunologic Mechanisms of Eosinophilic Esophagitis.Current allergy and asthma reports · 2016Review
- Neurotrophic tyrosine kinase receptor 1 is a direct transcriptional and epigenetic target of IL-13 involved in allergic inflammation.Mucosal immunology · 2015Article
- Genetic and epigenetic underpinnings of eosinophilic esophagitis.Gastroenterology clinics of North America · 2014Article
- Correlation of increased PARP14 and CCL26 expression in biopsies from children with eosinophilic esophagitis.The Journal of allergy and clinical immunology · 2014Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The etiology of a variety of chronic inflammatory disorders has been attributed to the interaction of genetic and environmental factors. Herein, we identified a link between epigenetic regulation and IL-13-driven eotaxin-3 in the pathogenesis of chronic allergic inflammation. We first demonstrated that the cAMP-responsive element (CRE) site in the eotaxin-3 promoter affects IL-13-induced eotaxin-3 promoter activity. Furthermore, the CRE-binding protein-binding protein (CBP), a histone acetyltransferase, induced base-line and IL-13-induced eotaxin-3 promoter activity. Additionally, IL-13 treatment promoted global histone 3 acetylation as well as the formation of a complex containing CBP and STAT6 and the subsequent acetylation of histone 3 at the eotaxin-3 promoter. CBP gene silencing decreased IL-13-induced transcription of eotaxin-3. Conversely, inhibition of histone deacetylation increased IL-13-induced eotaxin-3 production. Clinical studies demonstrated markedly increased global acetylation of histone 3 in the inflamed tissue of patients with allergic inflammation. Collectively, these results identify an epigenetic mechanism involving CBP and chromatin remodeling in regulating IL-13-induced chemokine transcription.
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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.