ß-catenin, a multifunctional protein stimulating several genes important for cell proliferation, is expressed in the heart. Signaling involving ß-catenin participates in directing cardiac development and in the pathophysiology of cardiac hypertrophy. Nothing is known, however, on the role of ß-catenin in the regulation of cardiac ion channels. The present study explored the interaction of ß-catenin and KCNE1/KCNQ1, the channel K⁺ channel complex underlying the repolarizing slowly activating outwardly rectifying K⁺ current IsK. To this end, KCNE1/KCNQ1 was expressed in Xenopus oocytes with and without ß-catenin and the depolarization- (up to 60 mV) induced current determined by using the two-electrode voltage clamp. As a result, beta catenin enhanced the KCNE1/KCNQ1-mediated current. In order to study whether ß-catenin is effective as a transcription factor, further experiments were done with actinomycin D, an inhibitor of transcription. As a result, the effect of ß-catenin on KCNE1/KCNQ1 mediated current was not affected by actinomycin D. Confocal microscopy revealed that ß-catenin enhanced the KCNE1/KCNQ1 protein abundance in the cell membrane. ß-catenin did not delay the decline of KCNE1/KCNQ1 mediated current following treatment of the oocytes with brefeldin A, which prevents insertion of new vesicles into the membrane. Thus, ß-catenin stimulated the insertion of KCNE1/KCNQ1 into the membrane rather than inhibiting the retrieval from the membrane. Taken together, ß-catenin is a positive regulator of KCNE1/KCNQ1 activity by stimulating the membrane insertion of this cardiac channel.