This study provides the first evidence of the critical role of the Nav1.5 N-terminal region in channel function and the dominant-negative effect of trafficking-defective channels via α-subunit interaction.
Should not yet inform clinical arrhythmia management; leaves open targeted modulation of Nav1.5 trafficking in future models.
This study reports for the first time the critical role of the Na(v)1.5 N-terminal region in channel function and the dominant-negative effect of trafficking-defective channels occurring through α-subunit interaction.
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Clatot et al. (2012) studied this question.
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