In-vitro the voltage-gated potassium channel member Q1 (KCNQ1) associates with the accessory subunit KCNE1 to form an outward current with kinetics closely resembling that of the cardiac slow delayed rectifier current (IKs) (Sanguinetti et al, 1996). The IKs current is involved in the repolarisation phase of the cardiac action potential. Defects in KCNQ1 are the cause of several inherited diseases that can cause disturbances in heart rhythm such as long QT syndrome (LQT1). The IKs channel complex is also a known cardiovascular liability for drugs that prolong the cardiac action potential, suggesting a role in acquired long QT-like disorders (Towart et al, 2009). The aim of this study was to characterise the IKs current in a transfected human cell line and to determine the distribution of KCNQ1 and KCNE1 in healthy human hearts. To characterise the IKs current whole-cell patch clamp recordings were obtained from Human Embryonic Kidney (HEK) 293 cells that were transiently transfected with plasmids (pCEP4) containing KCNQ1 (n=3) or KCNQ1 and KCNE1 (n=10) at a ratio of 1:1 (Fig. 1). Total RNA was extracted from 16 different areas (including atria, ventricles, aorta, pulmonary vein and septum) of non-diseased female human hearts (n=2) from organ donors that were technically unsuitable for transplantation and expression of KCNQ1 and KCNE1 mRNA characterised using end-point PCR. KCNQ1 only transfection produced a current with rapid activation kinetics whereas KCNQ1 and KCNE1 co-transfection produced a current that had much slower activation kinetics. PCR revealed that KCNQ1 and KCNE1 are differentially expressed in various regions of the heart. Both KCNQ1 and KCNE1 mRNA were expressed in most of the 16 areas examined, with the exception of the aorta and pulmonary vein which showed little or no expression. KCNQ1 expression was highest in the septum and AV (atrioventricular) node, with KCNE1 expression highest in septum, AV node and various regions in the left ventricle. As KCNQ1 and KCNE1 co-expression produces a current that closely resembles that of the cardiac IKs current, this demonstrates that KCNQ1 and KCNE1 together are vital in producing the kinetics required for the channel complex to be involved in cardiac repolarisation. The co-localisation of KCNQ1 and KCNE1 mRNA in the heart suggests a possible functional complex between these proteins. High levels of expression between KCNQ1 and KCNE1 in the left ventricle were expected, however, in the AV node and septum high levels of expression suggests an alternative role for the IKs channel complex, possibly in signal generation and/or transduction.