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Top of pageThe F508del CFTR mutant retains some residual channel functionWhen Rich et al11 found that expression of F508del CFTR in CF airway epithelial cells failed to correct the defective Cl permeability of these cells and Cheng et al12 subsequently demonstrated that the F508del mutation disrupts CFTR biosynthesis and membrane trafficking in COS 7 cells, it was widely assumed that F508del CFTR had no Cl channel function. Surprisingly however, Drumm et al13 demonstrated that F508del CFTR generates a cAMP activated Cl conductance when expressed in Xenopus oocytes. Because F508del CFTR Cl currents had similar conduction and permeation properties, but reduced magnitude compared with those of wild type CFTR, Drumm et al13 speculated that F508del CFTR forms a channel with attenuated sensitivity to cAMP agonists, a conclusion that was to prove prescient. Concurrently, Dalemans et al14 used the patch clamp technique to demonstrate that F508del CFTR forms a Cl channel regulated by cAMP dependent phosphorylation in Vero cells. However, there was one notable exception, the pattern of channel gating of F508del CFTR differed dramatically from that of wild type CFTR14.
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