C-terminal HERG mutations in LQT2 disrupt the functional coupling between beta-adrenergic stimulation and HERG channel activity mediated by 14-3-3epsilon, explaining the susceptibility to stress-induced arrhythmias.
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May explain stress-induced arrhythmia susceptibility in LQT2; leaves open whether targeting 14-3-3epsilon coupling offers therapeutic benefit.
Choe et al. (2006) studied this question.
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