A human genetic defect associated with 'long Q-T syndrome', an abnormality of 
cardiac rhythm involving the repolarization of the action potential, was 
recently found to lie in the HERG gene, which codes for a potassium channel. The 
HERG K+ channel is unusual in that it seems to have the architectural plan of 
the depolarization-activated K+ channel family (six putative transmembrane 
segments), yet it exhibits rectification like that of the inward-rectifying K+ 
channels, a family with different molecular structure (two transmembrane 
segments). We have studied HERG channels expressed in mammalian cells and find 
that this inward rectification arises from a rapid and voltage-dependent 
inactivation process that reduces conductance at positive voltages. The 
inactivation gating mechanism resembles that of C-type inactivation, often 
considered to be the 'slow inactivation' mechanism of other K+ channels. The 
characteristics of this gating suggest a specific role for this channel in the 
normal suppression of arrhythmias.