Key result
Calcified calmodulin N lobe and PIP2 compete for a binding site in helix B of the proximal Kv7.1 C terminus, suggesting a mechanism to limit excessive IKS current depression.
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Extends molecular model of IKS regulation; leaves open any role in arrhythmia risk or therapy.
Tobelaim et al. (2017) studied Long-QT syndrome. Calcified calmodulin N lobe and PIP2 was evaluated on Binding competition to helix B of the proximal Kv7.1 C terminus. Calcified calmodulin N lobe and PIP2 compete for a binding site in helix B of the proximal Kv7.1 C terminus, suggesting a mechanism to limit excessive IKS current depression.
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