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Research Article Free access | 10.1172/JCI113274
Cardiovascular Research Institute, University of California San Francisco 94143.
Find articles by Barthelson, R. in: JCI | PubMed | Google Scholar
Cardiovascular Research Institute, University of California San Francisco 94143.
Find articles by Widdicombe, J. in: JCI | PubMed | Google Scholar
Published December 1, 1987 - More info
Cl-impermeability in cystic fibrosis (CF) tracheal epithelium derives from a deficiency in the beta-adrenergic regulation of apical membrane Cl- channels. To test the possibility that cAMP-dependent kinase is the cause of this deficiency, we assayed this kinase in soluble fractions from cultured airway epithelial cells, including CF human tracheal epithelial cells. Varying levels of cAMP were used in these assays to derive both a Vmax and apparent dissociation constant (Kd) for the enzymes in soluble extracts. The cAMP-dependent protein kinase from CF human tracheal epithelial cells has essentially the same Vmax and apparent Kd as non-CF human, bovine, and dog tracheal epithelial cells. Thus, the total activity of the cAMP-dependent kinases and their overall responsiveness to cAMP are unchanged in CF.
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