Mutations in the hminK gene cause long QT syndrome and suppress lKs function
Author:
Publisher
Springer Science and Business Media LLC
Subject
Genetics
Link
http://www.nature.com/articles/ng1197-338.pdf
Reference17 articles.
1. Rettig, J. et al. Inactivation properties of voltage-gated K+ channels altered by presence of β-subunit. Nature 369, 289–294 (1994).
2. Shi, G. et al., β-subunits promote K+ channel surface expression through effects early in biosynthesis. Neuron 16, 843–852 (1996).
3. Sanguinetti, M.C. et al. Coassembly of KVLQT1 and minK (IsK) proteins to form cardiac IKs potassium channel. Nature 384, 80–83 (1996).
4. Barhanin, J. et al. KVLQT1 and IsK (minK) proteins associate to form the IKs cardiac potassium current. Nature 384, 78–80 (1996).
5. Wang, Q. et al. Positional cloning of a novel potassium channel gene: KVLQTl mutations cause cardiac arrhythmias. Nature Genet. 12, 17–23 (1996).
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