What is it about?
Cardiac channelopathies are cause of arrhythmias and sudden death and often arise by mutations in genes encoding ion channel subunits. Here we show that a family mutation in β2, a subunit of the voltage-gated sodium (NaV) channel, affects surface localization of the cardiac isoform NaV1.5.
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Why is it important?
Our findings add to the understanding of β2 role in NaV1.5 trafficking and localization. This influences cell excitability and electrical coupling in the heart. Thus, our data will contribute to knowledge on how arrhythmias develop.
Perspectives
The data from this paper were generated to the most part from work by three master’s students, which share co-authorship. Therefore, financial resources to cover the human cost can be considered zero.
Dr Marcel Verges
University of Girona
Read the Original
This page is a summary of: Trafficking and localisation to the plasma membrane of Nav
1.5 promoted by the β2 subunit is defective due to a β2 mutation associated with Brugada syndrome, Biology of the Cell, July 2017, Wiley,
DOI: 10.1111/boc.201600085.
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