ArticleAmerican journal of respiratory cell and molecular biology2015
Oxidative stress regulates CFTR gene expression in human airway epithelial cells through a distal antioxidant response element.
Article in American journal of respiratory cell and molecular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 49 citations in OpenAlex.
- Epigenetic regulation and chromatin organization in cystic fibrosis airways.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2026Review
- Review
- PM2.5 toxin benzo[a]pyrene induces life-limiting inflammation and oxidative stress in the airway by up-regulation of TRPC6 and inactivation of β2AR/CFTR signaling.bioRxiv : the preprint server for biology · 2026Article
- CFTR activity in nasal potential difference of adults with idiopathic bronchiectasis.Respiratory research · 2026Article
- CFTR Gene Regulation in Human Pancreatic Duct, Bile Duct and Sweat Gland Epithelial Cells.Journal of cellular and molecular medicine · 2025Article
- Ivacaftor attenuates gentamicin-induced ototoxicity through the CFTR-Nrf2-HO1/NQO1 pathway.Redox report : communications in free radical research · 2024Article
- A promoter-dependent upstream activator augments CFTR expression in diverse epithelial cell types.Biochimica et biophysica acta. Gene regulatory mechanisms · 2024Article
- Transcription factor BACH1 in cancer: roles, mechanisms, and prospects for targeted therapy.Biomarker research · 2024Review
- The impact of genomic distance on enhancer-promoter interactions at the CFTR locus.Journal of cellular and molecular medicine · 2024Article
- Tissue-Specific Regulation ofInternational journal of molecular sciences · 2023Review
- Cellular heterogeneity in the 16HBE14oPhysiological reports · 2023Article
- Article
- Cystic fibrosis transmembrane conductance regulator in COPD: a role in respiratory epithelium and beyond.The European respiratory journal · 2023Review
- Krüppel-Like Factor 5 Regulates CFTR Expression Through Repression by Maintaining Chromatin Architecture Coupled with Direct Enhancer Activation.Journal of molecular biology · 2022Article
- CFTR and Gastrointestinal Cancers: An Update.Journal of personalized medicine · 2022Review
- Article
- BACH1, the master regulator of oxidative stress, has a dual effect on CFTR expression.The Biochemical journal · 2021Article
- Dysfunction in the Cystic Fibrosis Transmembrane Regulator in Chronic Obstructive Pulmonary Disease as a Potential Target for Personalised Medicine.Biomedicines · 2021Review
- OTX2 regulates CFTR expression during endoderm differentiation and occupies 3' cis-regulatory elements.Developmental dynamics : an official publication of the American Association of Anatomists · 2021Article
- Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Cystic fibrosis transmembrane conductance regulator gene (CFTR) expression in human airway epithelial cells involves the recruitment of distal cis-regulatory elements, which are associated with airway-selective DNase hypersensitive sites at -44 kb and -35 kb from the gene. The -35-kb site encompasses an enhancer that is regulated by the immune mediators interferon regulatory factor 1 and 2 and by nuclear factor Y. Here we investigate the -44-kb element, which also has enhancer activity in vitro in airway epithelial cells but is inactive in intestinal epithelial cells. This site contains an antioxidant response element (ARE) that plays a critical role in its function in airway cell lines and primary human bronchial epithelial cells. The natural antioxidant sulforaphane (SFN) induces nuclear translocation of nuclear factor, erythroid 2-like 2 (Nrf2), a transcription factor that regulates genes with AREs in their promoters, many of which are involved in response to injury. Under normal conditions, the -44-kb ARE is occupied by the repressor BTB and CNC homology 1, basic leucine zipper transcription factor (Bach1), and v-Maf avian musculoaponeurotic fibrosarcoma oncogene homolog K (MafK) heterodimers. After 2 hours of SFN treatment, Nrf2 displaces these repressive factors and activates CFTR expression. Site-directed mutagenesis shows that both the ARE and an adjacent NF-κB binding site are required for activation of the -44-kb element in airway epithelial cells. Moreover, this element is functionally linked to the -35-kb enhancer in modulating CFTR expression in response to environmental stresses in the airway.
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Registered trials
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