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. 2015 Dec 1;113(2):E229–E238. doi: 10.1073/pnas.1514282112

Fig. S7.

Fig. S7.

KCNK1 does not contribute to the resting K+ current in PKD2L1 cells. (A) The current recorded from a KCNK1-AA-GFP–transfected HEK cell under conditions designed to unmask the current. Note that in 130 mM Rb+ (with 20 mM TEA), the current magnitude was much larger than that in 130 mM K+ extracellular solution (also with 20 mM TEA) as previously reported (57). Cs+ was not an effective blocker of KCNK1 current (58). (B) Same experiments as in A performed with a KIR2.1-transfected cell. Note that the current in Rb+ is much smaller than that in K+ solutions, and that Cs+ blocks the current effectively. (C) The current recorded in a PKD2L1 taste cell. Note that the current magnitude in Rb+ is smaller than that in K+, similar to the KIR2.1-mediated current. (D) The ratios of current in 130 mM Rb+ (IRb+) to that in 130 mM K+ (IK+) for KCNK1-AA, KIR2.1, and PKD2L1 taste cells. Using these data, we estimated the contribution of KCNK1 to the taste cell K+ current by rearranging a set of linear functions assuming that the inward currents in high Rb+ and K+ are generated solely from the contributions of KCNK1 and KIR2.1 (SI Methods). This calculation showed that KCNK1 accounts for no more than 1% of the resting K+ current.