Heteromeric KCNE2/KCNQ1 potassium channels in the luminal membrane of gastric parietal cells

Disruption of the K+ Channel β-Subunit KCNE3 Reveals an Important Role in Intestinal and Tracheal Cl− Transport

“…Our results agree with the observation that KCNQ1 traffics to the plasma membrane of transfected cell also without KCNE3, but KCNE3 needs KCNQ1 to reach that location (22). Whereas KCNQ1 homomultimers and KCNQ1/KCNE3 heteromers reside in basolateral membranes, heteromers formed of KCNQ1 with either KCNE1 (70) or KCNE2 (18) localize to the apical plasma membrane, suggesting a role for those ␤-subunits in targeting.…”

“…No changes in gastric morphology were observed in kcne3 Ϫ/Ϫ mice (supplemental Fig. S1, A and B), quite in contrast to the disruption of kcne2, which led to gastric glandular hyperplasia (19) and impaired acid secretion that depends on KCNQ1/KCNE2 channels in parietal cells (18,29).…”

“…4I), identifying them as parietal cells. These acid-secreting cells are known to express KCNE2 (18,29). By contrast, cells stained for KCNE3 were not positive for the H ϩ ,K ϩ -ATPase (Fig.…”

Functional Significance of K+ Channel β-Subunit KCNE3 in Auditory Neurons

“…For instance, Kv7.1 can be "converted" to a voltage-independent, constitutively active "leak" channel by associating with KCNE2 and KCNE3 (21, 38 -40). Such dichotomic behavior of Kv channels is crucial for providing K ϩ leak conductance in the colon and stomach (21,(41)(42)(43). However, such a phenomenon is exclusive to Kv7.1 due to the requirement of the S4 domain (44); other Kv7 subfamily ␣-subunits that reportedly interact with KCNEs do not become leak channels (i.e.…”

KCNE2 and the K+channel

“…[40][41][42][43][44] However, unlike KCNE3, KCNE2 also provides KCNQ1 with a property essential to its task in parietal cells-enhanced activation with low extracellular pH; in contrast, KCNQ1-KCNE3 channels are pH-insensitive, and homomeric KCNQ1 is inhibited by low pH. 45 Furthermore, in Kcne2-deleted mice, KCNQ1 traffics incorrectly, to the parietal cell basolateral membrane. This is because KCNE3, the expression of which is upregulated in Kcne2 2/2 mouse parietal cells, traffics KCNQ1 basolaterally in the absence of KCNE2 (Fig.…”