Why the study?
Despite advances in defining the pathophysiology of Nav1.5, the molecular mechanisms underlying its regulation by post-transcriptional regulators such as ncRNAs and its contribution to Brugada syndrome are poorly understood.
Design
Mini-review
Authors
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SCN5A mutations impair Nav1.5 function and link to severe arrhythmias; leaves open mutation-specific therapeutic targeting.
Key points are not available for this paper at this time.
Daimi et al. (2020) studied this question.
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