ArticleThe Biochemical journal2007
The epigenetic signature of CFTR expression is co-ordinated via chromatin acetylation through a complex intronic element.
Article in The Biochemical journal, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 30 citations in OpenAlex.
- Targeted Therapy for Restoring CFTR Activity: From Experimental to Clinical Features.International journal of molecular sciences · 2026Review
- Tissue-Specific Regulation ofInternational journal of molecular sciences · 2023Review
- Chasing a Breath of Fresh Air in Cystic Fibrosis (CF): Therapeutic Potential of Selective HDAC6 Inhibitors to Tackle Multiple Pathways in CF Pathophysiology.Journal of medicinal chemistry · 2022Review
- Article
- A Peptide-Nucleic Acid Targeting miR-335-5p Enhances Expression of Cystic Fibrosis Transmembrane Conductance Regulator (Biomedicines · 2021Article
- Interplay Between Ion Channels and the Wnt/β-Catenin Signaling Pathway in Cancers.Frontiers in pharmacology · 2020Review
- MicroRNAs and Long Non-coding RNAs in Genetic Diseases.Molecular diagnosis & therapy · 2019Review
- Cftr Modulates Wnt/β-Catenin Signaling and Stem Cell Proliferation in Murine Intestine.Cellular and molecular gastroenterology and hepatology · 2018Article
- CFTR mutation enhances Dishevelled degradation and results in impairment of Wnt-dependent hematopoiesis.Cell death & disease · 2018Article
- A Peptide Nucleic Acid against MicroRNA miR-145-5p Enhances the Expression of the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) in Calu-3 Cells.Molecules (Basel, Switzerland) · 2017Article
- Long Non-coding RNA BGas Regulates the Cystic Fibrosis Transmembrane Conductance Regulator.Molecular therapy : the journal of the American Society of Gene Therapy · 2016Article
- Analysis of long-range interactions in primary human cells identifies cooperative CFTR regulatory elements.Nucleic acids research · 2016Article
- CHD6 regulates the topological arrangement of the CFTR locus.Human molecular genetics · 2015Article
- A balance between activating and repressive histone modifications regulates cystic fibrosis transmembrane conductance regulator (CFTR) expression in vivo.Epigenetics · 2014Article
- Transcriptional networks driving enhancer function in the CFTR gene.The Biochemical journal · 2012Article
- Potential Agents for Treating Cystic Fibrosis: Cyclic Tetrapeptides that Restore Trafficking and Activity of ΔF508-CFTR.ACS medicinal chemistry letters · 2011Article
- Histone deacetylase: a potential therapeutic target for fibrotic disorders.The Journal of pharmacology and experimental therapeutics · 2010Review
- NF-E2-related factor 2, a key inducer of antioxidant defenses, negatively regulates the CFTR transcription.Cellular and molecular life sciences : CMLS · 2010Article
- A complex intronic enhancer regulates expression of the CFTR gene by direct interaction with the promoter.Journal of cellular and molecular medicine · 2009Article
- An insulator element 3' to the CFTR gene binds CTCF and reveals an active chromatin hub in primary cells.Nucleic acids research · 2009Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The CFTR (cystic fibrosis transmembrane conductance regulator) gene is a tightly regulated and differentially expressed transcript in many mucosal epithelial cell types. It appears that DNA sequence variations alone do not explain CFTR-related gastrointestinal disease patterns and that epigenetic modifiers influence CFTR expression. Our aim was to characterize the native chromatin environment in cultured cells for intestinal CFTR expression by determining the relationship between histone acetylation and occupation of CFTR by multiple transcription factors, through a common regulatory element. We used HDAC (histone deacetylase) inhibition and ChIP (chromatin immunoprecipitation) analyses to define regions associated with acute acetylation of histone at the CFTR locus. We identified a region within the first intron associated with acute acetylation of histone H4 as an epigenetic signature corresponding to an intestine-specific enhancer element for CFTR. DHS (DNase I-hypersensitivity) assays and ChIP were used to specify control elements and occupation by regulatory factors. Quantitative ChIP procedures indicate that HNF1alpha (hepatic nuclear factor 1alpha) and Cdx2 (caudal homeobox protein 2) occupy and regulate through a novel intronic enhancer element of CFTR and that Tcf4 (T-cell factor 4) overlaps the same DNA element. RNAi (RNA interference) of Tcf4 and HNF1alpha decreased intestinal cell CFTR expression, identifying these as positive regulatory factors and CFTR as a target for Wnt signalling. We have linked the acetylation signature of nucleosomal histones to active intestinal CFTR expression and occupation by transcription factors HNF1alpha, Cdx2 and Tcf4 which converge to modify chromatin architecture. These studies suggest the therapeutic potential of histone modification strategies, such as inhibition of HDAC activity, to treat CFTR-associated disease by selectively enhancing CFTR expression.
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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.