Key result
Co-expression of SCN3b with SCN5a resulted in a threefold increase in functional sodium channel expression and caused a significant depolarising shift in steady-state inactivation.
SCN3b is heterogeneously expressed in the heart and modulates the kinetics of the cardiac sodium channel SCN5a, which may have important consequences for cardiac electrical activity.
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Caution against clinical translation of SCN3b modulation; leaves open its role in human cardiac sodium channelopathies pending mammalian validation.
Fahmi et al. (2001) studied this question. SCN3b co-expression with SCN5a vs. SCN5a alone or SCN5a + SCN1b was evaluated on Sodium channel expression and kinetics. Co-expression of SCN3b with SCN5a resulted in a threefold increase in functional sodium channel expression and caused a significant depolarising shift in steady-state inactivation.
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