Coassembly of K(sub v)LQT1 and minK (IsK) proteins to form cardiac I(sub Ks) potassium channel

The potassium (K+) channel gene K(sub v)LQT1 coassembles with the 130-amino acid protein minK to form the cardiac I(sub Ks) potassium channel. The minK protein has a single putative transmembrane domain and fails to form functional channels without help of the LQT1 gene. The two delayed-rectifier K+ currents, I(sub Kr) and I(sub Ks) are responsible for the modulation of the action-potential duration in cardiac myocytes. Mutations in the LQT1 gene and dysfunctions of the I(sub Ks) channel leads to cardiac arrhythmias.