Article
Long QT2 mutation on the Kv11.1 ion channel inhibits current activity by ablating a protein kinase Cα consensus site.
Molecular pharmacology - 1 Sept 2012
Donovan Alexander J, Lansu Katherine, Williams Jason G, Denning Mitchell F, Gentile Saverio
Abstract excerpt
Mutations that inhibit Kv11.1 ion channel activity contribute to abnormalities of cardiac repolarization that can lead to long QT2 (LQT2) cardiac arrhythmias and sudden death. However, for most of these mutations, nothing is known about the molecular mechanism linking Kv11.1 malfunction to cardiac death. We have previously demonstrated that disease-related mutations that create consensus sites for kinases on ion...
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