Model of effects of Kcne2/Kcne3 knockout in mouse parietal cells. Model (from [141]) showing the putative short-circuit current in parietal cells of Kcne2 −/− mice (b) compared to Kcne2 +/+ mice (a). This is hypothesized to arise from the previously observed switch in KCNQ1 trafficking from apical (Kcne2 +/+, (a)) to basolateral because of KCNE3 upregulation (b) [141]. In double-knockout Kcne2 −/−Kcne3 −/− mice, KCNQ1 is apical but presumed nonfunctional because it lacks KCNE2 and KCNE3, which confer constitutive activation and limit inactivation (c) [141].
