ArticleProceedings of the National Academy of Sciences of the United States of America1995
Basal expression of the cystic fibrosis transmembrane conductance regulator gene is dependent on protein kinase A activity.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1995. 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, 61 citations in OpenAlex.
- Upregulation of CFTR Protects against Palmitate-Induced Endothelial Dysfunction by Enhancing Autophagic Flux.Oxidative medicine and cellular longevity · 2020Article
- Current insights into the role of PKA phosphorylation in CFTR channel activity and the pharmacological rescue of cystic fibrosis disease-causing mutants.Cellular and molecular life sciences : CMLS · 2017Review
- Review
- A balance between activating and repressive histone modifications regulates cystic fibrosis transmembrane conductance regulator (CFTR) expression in vivo.Epigenetics · 2014Article
- IL-8 inhibits cAMP-stimulated alveolar epithelial fluid transport via a GRK2/PI3K-dependent mechanism.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013Article
- CFTR activity and mitochondrial function.Redox biology · 2013Review
- Phosphorylation-dependent 14-3-3 protein interactions regulate CFTR biogenesis.Molecular biology of the cell · 2012Article
- Nucleosome occupancy reveals regulatory elements of the CFTR promoter.Nucleic acids research · 2012Article
- Glutathione in cancer cell death.Cancers · 2011Article
- Multiple mechanisms influence regulation of the cystic fibrosis transmembrane conductance regulator gene promoter.American journal of respiratory cell and molecular biology · 2010Article
- Mitigation of chlorine lung injury by increasing cyclic AMP levels.Proceedings of the American Thoracic Society · 2010Review
- Cell-type-specific long-range looping interactions identify distant regulatory elements of the CFTR gene.Nucleic acids research · 2010Article
- Transforming growth factor beta1 inhibits cystic fibrosis transmembrane conductance regulator-dependent cAMP-stimulated alveolar epithelial fluid transport via a phosphatidylinositol 3-kinase-dependent mechanism.The Journal of biological chemistry · 2010Article
- A complex intronic enhancer regulates expression of the CFTR gene by direct interaction with the promoter.Journal of cellular and molecular medicine · 2009Article
- Binding of serum response factor to cystic fibrosis transmembrane conductance regulator CArG-like elements, as a new potential CFTR transcriptional regulation pathway.Nucleic acids research · 2005Article
- HNF1alpha is involved in tissue-specific regulation of CFTR gene expression.The Biochemical journal · 2004Article
- Tumor necrosis factor-alpha/interleukin-10 balance in normal and cystic fibrosis children.Mediators of inflammation · 2001Article
- Comparative genomic sequence analysis of the human and mouse cystic fibrosis transmembrane conductance regulator genes.Proceedings of the National Academy of Sciences of the United States of America · 2000Article
- Regulation and expression of multidrug resistance (MDR) transcripts in the intestinal epithelium.British journal of cancer · 1999Article
- Aspirin and some other nonsteroidal anti-inflammatory drugs inhibit cystic fibrosis transmembrane conductance regulator protein gene expression in T-84 cells.Mediators of inflammation · 1999Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The cystic fibrosis transmembrane conductance regulator (CFTR) functions as a Cl- channel that becomes activated after phosphorylation by cAMP-dependent protein kinase (PKA). We demonstrate that PKA also plays a crucial role in maintaining basal expression of the CFTR gene in the human colon carcinoma cell line T84. Inhibition of PKA activity by expression of a dominant-negative regulatory subunit or treatment with the PKA-selective inhibitor N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide (H-89) caused a complete suppression of CFTR gene expression without affecting other constitutively active genes. Basal expression of a 2.2-kb region of the CFTR promoter linked to a luciferase reporter gene (CFTR-luc) exhibited the same dependence on PKA. The ability of cAMP to induce CFTR over basal levels is cell-type specific. In T84 cells, both the endogenous CFTR gene and CFTR-luc exhibited only a modest inducibility (approximately 2-fold), whereas in the human choriocarcinoma cell line JEG-3, CFTR-luc could be induced at least 4-fold. A variant cAMP-response element is present at position -48 to -41 in the CFTR promoter, and mutation of this sequence blocks basal expression. We conclude that cAMP, acting through PKA, is an essential regulator of basal CFTR gene expression and may mediate an induction of CFTR in responsive cell types.
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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.