In contrast to other members of the Eag family of voltage-gated, outwa
rdly rectifying potassium channels, the human eag-related gene (HERG)
has now been shown to encode an inwardly rectifying potassium channel.
The properties of HERG channels are consistent with the gating proper
ties of Eag-related and other outwardly rectifying, S4-containing pota
ssium channels, but with the addition of an inactivation mechanism tha
t attenuates potassium efflux during depolarization. Because mutations
in HERG cause a form of long-QT syndrome, these properties of HERG ch
annel function may be critical to the maintenance of normal cardiac rh
ythmicity.