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Regulation of epithelial chloride flux, which is defective in patients with cystic fibrosis, may be mediated by phosphorylation of the cystic fibrosis transmembrane conductance regulator (CFTR) by cyclic AMP-dependent protein kinase (PKA) or protein kinase C (PKC). CFTR regulates both HCO(3)(-) secretion and HCO(3)(-) salvage in secretory epithelia.
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