© 1999 American Heart Association, Inc.
Editorial |
Molecular Identity of Ito
Kv1.4 Redux
From the Department of Neurobiology and Behavior, State University of New York at Stony Brook, Stony Brook, NY.
Correspondence to Dr David McKinnon, Department of Neurobiology and Behavior, State University of New York at Stony Brook, Stony Brook, NY 11794-5230. E-mail dmckinnon@epo.som.sunysb.edu
Key Words: K+ channel • transient outward current • molecular biology
Our understanding of the function of the Kv1.4 K+ channel in cardiac physiology has changed over time. The Kv1.4 gene was the first mammalian gene identified that encoded a rapidly inactivating or transient K+ channel.1 2 Previous attempts at cloning mammalian K+ channels based on homology to the Drosophila Shaker gene, which encodes a rapidly inactivating channel, had unexpectedly turned up several delayed rectifier channels. There were high expectations, therefore, when the Kv1.4 gene was shown to encode a transient channel, and it was quite reasonably suggested that the Kv1.4 channel could underlie the transient outward K+ current (Ito) in cardiac muscle.2 A rival for the affections of Ito aficionados soon appeared, however, with the identification of a second family of transient channels, which contained two members known as Kv4.1 and Kv4.2.3 4 On the basis of the observation that the Kv4.2 gene was expressed in heart, it was suggested that these channels also might underlie the Ito.5
Initial interest in the molecular basis of the
Ito focused almost exclusively on
Kv1.4,6 7 8 however, and the Kv4.2 channel languished
largely unnoticed. There were several reasons for this. The Kv4.2
channel, when expressed in Xenopus oocytes, was something of
an ugly duckling. It activated more slowly than
Ito, and its inactivation phase was complex
and incomplete, with multiple inactivation rates and a
noninactivating sustained
component.4 This unfavorable aesthetic appearance was
largely due to the limitations of the Xenopus oocyte
expression system used in the initial studies, which appears to lack
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