ArticleMolecular and cellular biology2013
Immune mediators regulate CFTR expression through a bifunctional airway-selective enhancer.
Article in Molecular and cellular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 34 citations in OpenAlex.
- CFTR activity in nasal potential difference of adults with idiopathic bronchiectasis.Respiratory research · 2026Article
- Distinct regulatory elements of SLC6A14 expression contribute to modification of cystic fibrosis phenotypes.Human genetics · 2026Article
- CFTR Gene Regulation in Human Pancreatic Duct, Bile Duct and Sweat Gland Epithelial Cells.Journal of cellular and molecular medicine · 2025Article
- Molecular mechanism analysis of nontuberculous mycobacteria infection in patients with cystic fibrosis.Future microbiology · 2024Article
- A promoter-dependent upstream activator augments CFTR expression in diverse epithelial cell types.Biochimica et biophysica acta. Gene regulatory mechanisms · 2024Article
- 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
- Krüppel-Like Factor 5 Regulates CFTR Expression Through Repression by Maintaining Chromatin Architecture Coupled with Direct Enhancer Activation.Journal of molecular biology · 2022Article
- Article
- Epigenome editing of the CFTR-locus for treatment of cystic fibrosis.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2022Article
- Revisiting CFTR Interactions: Old Partners and New Players.International journal of molecular sciences · 2021Review
- BACH1, the master regulator of oxidative stress, has a dual effect on CFTR expression.The Biochemical journal · 2021Article
- 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
- Looping of upstream cis-regulatory elements is required for CFTR expression in human airway epithelial cells.Nucleic acids research · 2020Article
- Genetic variation in CFTR and modifier loci may modulate cystic fibrosis disease severity.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2020Review
- A BAC Transgene Expressing Human CFTR under Control of Its Regulatory Elements Rescues Cftr Knockout Mice.Scientific reports · 2019Article
- Cell-Selective Regulation of CFTR Gene Expression: Relevance to Gene Editing Therapeutics.Genes · 2019Review
- Screening for Regulatory Variants in 460 kb Encompassing the CFTR Locus in Cystic Fibrosis Patients.The Journal of molecular diagnostics : JMD · 2019Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
An airway-selective DNase-hypersensitive site (DHS) at kb -35 (DHS-35kb) 5' to the cystic fibrosis transmembrane conductance regulator (CFTR) gene is evident in many lung cell lines and primary human tracheal epithelial cells but is absent from intestinal epithelia. The DHS-35kb contains an element with enhancer activity in 16HBE14o- airway epithelial cells and is enriched for monomethylated H3K4 histones (H3K4me1). We now define a 350-bp region within DHS-35kb which has full enhancer activity and binds interferon regulatory factor 1 (IRF1) and nuclear factor Y (NF-Y) in vitro and in vivo. Small interfering RNA (siRNA)-mediated depletion of IRF1 or overexpression of IRF2, an antagonist of IRF1, reduces CFTR expression in 16HBE14o- cells. NF-Y is critical for maintenance of H3K4me1 enrichment at DHS-35kb since depletion of NF-YA, a subunit of NF-Y, reduces H3K4me1 enrichment at this site. Moreover, depletion of SETD7, an H3K4 monomethyltransferase, reduces both H3K4me1 and NF-Y occupancy, suggesting a requirement of H3K4me1 for NF-Y binding. NF-Y depletion also represses Sin3A and reduces its occupancy across the CFTR locus, which is accompanied by an increase in p300 enrichment at multiple sites. Our results reveal that the DHS-35kb airway-selective enhancer element plays a pivotal role in regulation of CFTR expression by two independent regulatory mechanisms.
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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.