Key result
A single point mutation (N406K) in the human cardiac Na+ channel significantly reduced the inhibitory effect of eicosapentaenoic acid on sodium currents compared to wild-type channels.
The asparagine at site 406 in the human cardiac sodium channel alpha subunit is critical for the inhibition of cardiac voltage-gated Na+ currents by polyunsaturated fatty acids, providing a mechanistic basis for their antiarrhythmic effects.
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N406 may mediate PUFA Na+ channel inhibition in vitro; hypothesis-generating for antiarrhythmic mechanisms, with no clinical implications yet.
Xiao et al. (2001) studied In vitro study of human cardiac Na+ channels. Eicosapentaenoic acid (EPA) vs. Wild-type vs mutant channels was evaluated on Inhibition of INa by EPA. A single point mutation (N406K) in the human cardiac Na+ channel significantly reduced the inhibitory effect of eicosapentaenoic acid on sodium currents compared to wild-type channels.
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