IN mammalian cardiac cells, a variety of transient or sustained K⁺ currents contribute to the repolarization of action potentials¹. There are two main components of the delayed-rectifier sustained K⁺ current, I_Kr (rapid) and I_KS (slow)². I_Kr is the product of the gene HERG^3,4 which is altered in the long-QT syndrome, LQT2 (ref. 5). A channel with properties similar to those of the I_KS channel is produced when the cardiac protein IsK is expressed in Xenopus oocytes^6–8. However, it is a small protein with a very unusual structure for a cation channel^9–15. The LQT1 gene is another gene associated with the LQT syndrome, a disorder that causes sudden death from ventricular arrhythmias¹⁶. Here we report the cloning of the full-length mouse K_VLQT1 complemen-tary DNA and show that K_VLQT1 associates with IsK to form the channel underlying the I_KS cardiac current, which is a target of class-Ill anti-arrhythmic drugs and is involved in the LQT₁ syndrome.