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. 2007 Sep;18(9):3388–3397. doi: 10.1091/mbc.E07-02-0126

Figure 5.

Figure 5.

Impact of complex disruption on whole cell outwardly rectifying and CFTR mediated Cl− currents in 16HBE14o− stimulated with FSK/IBMX. (A) Outwardly rectifying and CFTR-mediated Cl− currents in 16HBE14o− cells stimulated with FSK/IBMX for 30 min. Whole cell currents recorded from a typical cell under the control circumstance and in the presence of 500 μM DIDS and 500 μM DIDS plus 10 μM CFTRihn172. Clamp potential was stepped from −40 mV to between +100 and −100 mV, in −20 mV steps. (B) Effect of CaN inhibitors cypermethrin (5 nM) and cyclosporin A (1 μM) on ICFTR. Cells were incubated with CaN inhibitors for 5 min before exposure to FSK/BMX plus inhibitor for 30 min. Control currents for each data set were day matched. CaN inhibitors inhibited the cAMP/PKA-dependent CFTR, but not ORCC, activity. (C and D) Effect of Ac1-14 and N1-14 on IDIDS and ICFTR. Cells were incubated for 30 min in the presence of peptide, followed by incubation with the peptide plus FSK/IBMX for 30 min. Control currents for each data set were day matched, with control cells incubated for 30 min in control solution, followed by 30 min in the presence of FSK/IBMX. Ac1-14, but not N1-14, inhibited both the cAMP/PKA-dependent ORCC and CFTR activities. (E) Effect of Ac1-14 and N1-14 on SCC in gut epithelia. SCC measurements were obtained, in the presence or absence of Ac1-14 or N1-14 (100 μM), in response to Ach and glucose stimulation of mounted gut epithelia biopsies (n = 3). **p < 0.05, ANOVA.