KCNQ1 (KvLQT1) gene encodes a 6-TM channel protein which form functional K+ channels together with the b-subunit encoded by KCNE1 that forms current similar to IKs in heart cells. Previous experiments have demonstrated that mutations in KCNQ1 and /or KCNE1 can result in long Q-T syndromes. In TRa1 and TRa1b deficient mice the expression of KCNE1 is stimulated but the animal unexpectedly have increased Q-T times and decreased heart rate. The present study was undertaken to test the hypothesis that overexpression of KCNE1 might affect the normal function of the KCNQ1-KCNE1 channel/current. In the present experiments Chinese hamster ovary (CHO) cells cells were transfected with a fixed amount of KCNQ1 cDNA together with an increasing amount of cDNA for the KCNE1 subunit. Patch clamp recordings from CHO cells showed that the outward rectifying current was maximal at a KCNE1:KCNQ1 stoichiometry of 1 whereas stoichiometries of KCNE1:KCNQ1 > 1 gave progressively smaller currents (conductances). A 90% reduction was seen at 3 KCNE1:KCNQ1. No changes in activation or deactivation of the channels were observed. Also there was no indication of changed ion selectivity. Possible effects to explain the result could be that either excess of KCNE1 decreases incorporation of KCNQ1 channels in plasma membrane or excess KCNE1 functionally occlude the channel. From structural arguments it can be argued that in a situation where many KCNE1 subunits are available this leads to an occlusion of the pore.