Defective regulation of outwardly rectifying Cl- channels by protein kinase A corrected by insertion of CFTR

The expression of recombinant cystic fibrosis (CF) genes by means of adeno-associated virus vectors in CF bronchial epithelial cells stops the defective Cl- secretion, produces conductance Cl- channels and revives protein kinase A stimulation of outwardly rectifying Cl- channels. Hence it may be possible to use gene expression to treat CF, a severe genetic disease that results from a defective gene for the cystic fibrosis transmembrane conductance regulator protein.