Article
An LQT mutant minK alters KvLQT1 trafficking.
American journal of physiology. Cell physiology - 1 Jun 2004
Krumerman Andrew, Gao Xiaohong, Bian Jin-Song, Melman Yonathan F, Kagan Anna, McDonald Thomas V
Abstract excerpt
Cardiac I(Ks), the slowly activated delayed-rectifier K(+) current, is produced by the protein complex composed of alpha- and beta-subunits: KvLQT1 and minK. Mutations of genes encoding KvLQT1 and minK are responsible for the hereditary long QT syndrome (loci LQT1 and LQT5, respectively). MinK-L51H fails to traffic to the cell surface, thereby failing to produce effective I(Ks). We examined the effects that...
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