Biophysical interactions of PIP2 and calmodulin with KCNQ (Kv7) K ion channels + KCNQ potassium channels control cellular excitability, and inherited mutations in the proximal half of the C- terminus of these membrane proteins can result in cardiac arrhythmia, deafness and epilepsy. The signature 'M-current' produced by KCNQ channels was first observed in sympathetic neurons, and can be inhibited by stimulation of Gq/11 muscarinic receptors.
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