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Trafficking and Function of the Voltage-Gated Sodium Channel β2 Subunit

by Eric Cortada 1,2, Ramon Brugada 1,2,3,4 and Marcel Verges 1,2,3,*
1
Cardiovascular Genetics Group, Girona Biomedical Research Institute (IDIBGI), C/ Doctor Castany, s/n—Edifici IDIBGI, 17190 Girona, Spain
2
Biomedical Research Networking Center on Cardiovascular Diseases (CIBERCV), 28029 Madrid, Spain
3
Medical Sciences Department, University of Girona Medical School, 17003 Girona, Spain
4
Cardiology Department, Hospital Josep Trueta, 17007 Girona, Spain
*
Author to whom correspondence should be addressed.
Biomolecules 2019, 9(10), 604; https://doi.org/10.3390/biom9100604
Received: 17 September 2019 / Revised: 7 October 2019 / Accepted: 8 October 2019 / Published: 13 October 2019
The voltage-gated sodium channel is vital for cardiomyocyte function, and consists of a protein complex containing a pore-forming α subunit and two associated β subunits. A fundamental, yet unsolved, question is to define the precise function of β subunits. While their location in vivo remains unclear, large evidence shows that they regulate localization of α and the biophysical properties of the channel. The current data support that one of these subunits, β2, promotes cell surface expression of α. The main α isoform in an adult heart is NaV1.5, and mutations in SCN5A, the gene encoding NaV1.5, often lead to hereditary arrhythmias and sudden death. The association of β2 with cardiac arrhythmias has also been described, which could be due to alterations in trafficking, anchoring, and localization of NaV1.5 at the cardiomyocyte surface. Here, we will discuss research dealing with mechanisms that regulate β2 trafficking, and how β2 could be pivotal for the correct localization of NaV1.5, which influences cellular excitability and electrical coupling of the heart. Moreover, β2 may have yet to be discovered roles on cell adhesion and signaling, implying that diverse defects leading to human disease may arise due to β2 mutations. View Full-Text
Keywords: cardiac arrhythmias; protein trafficking; voltage-gated sodium channel; NaV1.5; SCN2B cardiac arrhythmias; protein trafficking; voltage-gated sodium channel; NaV1.5; SCN2B
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Cortada, E.; Brugada, R.; Verges, M. Trafficking and Function of the Voltage-Gated Sodium Channel β2 Subunit. Biomolecules 2019, 9, 604.

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