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. 2018 May 14;13(5):e0196512. doi: 10.1371/journal.pone.0196512

Fig 6. CLCA2 enhances IClCa in TMEM16A-transduced HEK293 cells.

Fig 6

Representative whole-cell chloride currents from cells stably expressing vector (A), CLCA2 (B), TMEM16A plus vector (D) or CLCA2 plus TMEM16A (E) are shown. ICaCC was induced by application of 2 micromolar ionomycin in the presence of extracellular calcium. When the current peaked, a voltage ramp from -60 to +60mV was applied and the current response was recorded. In A and B, current was blocked by DIDS, 100 micromolar. In both D and E, current was fully inhibited by substitution of sodium gluconate (S.G.) for chloride. C, F, relative current amplitudes at +60mV +/- S.E.M. C, n = 9 for CLCA2; n = 7 for vector control; **, p<0.01. F, n = 4 cells for each condition; *, p = 0.02; **, p<0.01. The reversal potential was -8mV in agreement with the Nernst prediction of -7.56mV, based on an excess of 34mM chloride in the extracellular buffer.