Objective: In the heart, the voltage- activated KCNQ1 potassium channel is co- expressed with the accessory KCNE1 protein (b- subunit). The heteromeric KCNQ1/KCNE1 channel complex gives rise to the cardiac IKs delayed rectifier potassium current which is important for repolarization of the cardiomyocyte membrane. KCNE1 affects KCNQ1 function in two ways: it modulates the kinetic characteristics of the KCNQ1 current, and it augments the KCNQ1 current. This increase in macroscopic current could be due either to an increase in (i) the single-channel conductance, (ii) the open state probability, or (iii) the number of KCNQ1 channels in the membrane. In the present study we investigated whether the number of KCNQ1 channels present in the membrane is affected by co-expression of KCNE1. Methods: We quantified the level of KCNQ1 surface expression by using enzyme immunoassay. To do this, we employed a HA-tagged version of the KCNQ1 channel and expressed it with and without KCNE1 in Xenopus oocytes. The HA-tag, which is located at the second extracellular loop of the protein, allows us to "count" the number of KCNQ1 channels expressed in the cell membrane. In parallel, whole-oocyte currents were measured with two electrode voltage clamp. Results: The results show that the KCNQ1 surface expression is reduced by approximately 70 % when KCNE1 is co-expressed in the oocyte membrane despite that the current for the heteromeric KCNQ1/KCNE1 is increased by approximately 20 %. Conclusion: This observation indicates that the increase in the KCNQ1 current, when KCNE1 is co-expressed in Xenopus oocytes, is not due to an increase in ion channel number in the oocyte membrane, but rather to an increase in single- channel conductance or, perhaps more likely, an increase in open state probability.