ArticleAmerican journal of physiology. Lung cellular and molecular physiology2010
Modulation of endocytic trafficking and apical stability of CFTR in primary human airway epithelial cultures.
Article in American journal of physiology. Lung cellular and molecular physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 81 citations in OpenAlex.
- Cystic fibrosis transmembrane conductance regulator recruitment to phagosomes in neutrophils.Journal of innate immunity · 2013Trial
- Targeted recruitment of USP15 enhances CTLA4 surface levels and restricts its degradation.Life science alliance · 2026Article
- Neutrophil store-operated CaJournal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2025Article
- Cell type-specific regulation of CFTR trafficking-on the verge of progress.Frontiers in cell and developmental biology · 2024Review
- Cross-talk between CFTR and sphingolipids in cystic fibrosis.FEBS open bio · 2023Review
- Secretory Cells Dominate Airway CFTR Expression and Function in Human Airway Superficial Epithelia.American journal of respiratory and critical care medicine · 2021Article
- Alteration of Membrane Cholesterol Content Plays a Key Role in Regulation of Cystic Fibrosis Transmembrane Conductance Regulator Channel Activity.Frontiers in physiology · 2021Article
- In vitro 3D culture lung model from expanded primary cystic fibrosis human airway cells.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2020Article
- Exercise and Cystic Fibrosis.Advances in experimental medicine and biology · 2020Review
- CK19 stabilizes CFTR at the cell surface by limiting its endocytic pathway degradation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Activity of lumacaftor is not conserved in zebrafish Cftr bearing the major cystic fibrosis-causing mutation.FASEB bioAdvances · 2019Article
- Article
- Transcytosis maintains CFTR apical polarity in the face of constitutive and mutation-induced basolateral missorting.Journal of cell science · 2019Article
- Cyclodextrins reduce the ability of Pseudomonas aeruginosa outer-membrane vesicles to reduce CFTR ClAmerican journal of physiology. Lung cellular and molecular physiology · 2019Article
- The N terminus of α-ENaC mediates ENaC cleavage and activation by furin.The Journal of general physiology · 2018Article
- Lipid Nanoparticle-Delivered Chemically Modified mRNA Restores Chloride Secretion in Cystic Fibrosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2018Article
- Recent progress in translational cystic fibrosis research using precision medicine strategies.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2018Review
- Peripheral Protein Quality Control as a Novel Drug Target for CFTR Stabilizer.Frontiers in pharmacology · 2018Review
- Development of a High-Throughput Flow Cytometry Assay to Monitor Defective Trafficking and Rescue of Long QT2 Mutant hERG Channels.Frontiers in physiology · 2018Article
- From the endoplasmic reticulum to the plasma membrane: mechanisms of CFTR folding and trafficking.Cellular and molecular life sciences : CMLS · 2017Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 4 countries.
Funding
Abstract
CFTR is a highly regulated apical chloride channel of epithelial cells that is mutated in cystic fibrosis (CF). In this study, we characterized the apical stability and intracellular trafficking of wild-type and mutant CFTR in its native environment, i.e., highly differentiated primary human airway epithelial (HAE) cultures. We labeled the apical pool of CFTR and subsequently visualized the protein in intracellular compartments. CFTR moved from the apical surface to endosomes and then efficiently recycled back to the surface. CFTR endocytosis occurred more slowly in polarized than in nonpolarized HAE cells or in a polarized epithelial cell line. The most common mutation in CF, DeltaF508 CFTR, was rescued from endoplasmic reticulum retention by low-temperature incubation but transited from the apical membrane to endocytic compartments more rapidly and recycled less efficiently than wild-type CFTR. Incubation with small-molecule correctors resulted in DeltaF508 CFTR at the apical membrane but did not restore apical stability. To stabilize the mutant protein at the apical membrane, we found that the dynamin inhibitor Dynasore and the cholesterol-extracting agent cyclodextrin dramatically reduced internalization of DeltaF508, whereas the proteasomal inhibitor MG-132 completely blocked endocytosis of DeltaF508. On examination of intrinsic properties of CFTR that may affect its apical stability, we found that N-linked oligosaccharides were not necessary for transport to the apical membrane but were required for efficient apical recycling and, therefore, influenced the turnover of surface CFTR. Thus apical stability of CFTR in its native environment is affected by properties of the protein and modulation of endocytic trafficking.
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