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. 2009 Feb 27;284(9):5645–5653. doi: 10.1074/jbc.M806780200

FIGURE 5.

FIGURE 5.

Functional role of AMPK-regulation of CFTR. A, activation of CFTR whole cell conductance by stimulation with 20 μm forskolin (left column pair, raw baseline data in lower panel), 1 mm IBMX, 80 μm forskolin (middle column), and 5 mm IBMX, 2 μm forskolin, and 3 mm 8Br–-cAMP (right column). Increase of CFTR whole cell conductance by compound C (80 μm) relative to CFTR baseline conductance (upper panels). B, inactivation of CFTR whole cell conductances in oocytes expressing CFTR, CFTR, and AMPKα1β1γ1, or the catalytically dead mutant AMPKα1-K45R. C, inactivation of conductances generated by wtCFTR and S737A/S768A-CFTR. D, CFTR whole cell conductances activated by 3 mm Br–-cAMP, 3 mm Br–-cAMP, and 2 μm forskolin, or 3 mm Br–-cAMP and 2 μm forskolin and 1 mm IBMX, and effects of compound C. E, activation of CFTR by forskolin (2 μm) and additional stimulation by rolipram (50 μm), dipyridamol (80 μm), and IBMX (1 mm). Membrane currents were measured by voltage clamping in intervals from –60 to +40 mV, in steps of 10 mV. *, significant difference when compared with control. #, significant difference when compared with wtCFTR. Data are shown as mean ± S.E. (number of experiments).