Epithelial cell chloride channel activity correlates with improved airway function in cystic fibrosis patients with the major mutant: Delta F508.
- 1 November 2002
- journal article
- editorial
- Published by Springer Nature in Pediatric Research
- Vol. 52 (5) , 625-7
Abstract
No abstract availableKeywords
This publication has 29 references indexed in Scilit:
- Cystic Fibrosis as a Disease of Misprocessing of the Cystic Fibrosis Transmembrane Conductance Regulator GlycoproteinThe American Journal of Human Genetics, 1999
- Molecular insights into the physiology of the ‘thin film’ of airway surface liquidThe Journal of Physiology, 1999
- Correlation between nasal potential difference measurements, genotype and clinical condition in patients with cystic fibrosisEuropean Respiratory Journal, 1997
- Evidence for safety and efficacy of DOTAP cationic liposome mediated CFTR gene transfer to the nasal epithelium of patients with cystic fibrosisGene Therapy, 1997
- Modulation of disease severity in cystic fibrosis transmembrane conductance regulator deficient mice by a secondary genetic factorNature Genetics, 1996
- Glycerol Reverses the Misfolding Phenotype of the Most Common Cystic Fibrosis MutationJournal of Biological Chemistry, 1996
- The cystic fibrosis mutation (ΔF508) does not influence the chloride channel activity of CFTRNature Genetics, 1993
- Processing of mutant cystic fibrosis transmembrane conductance regulator is temperature-sensitiveNature, 1992
- Mislocalization of ΔF508 CFTR in cystic fibrosis sweat glandNature Genetics, 1992
- Independent genetic determinants of pancreatic and pulmonary status in cystic fibrosisThe Lancet, 1990