Abstract Nav1. 5, the pore forming α-subunit of the voltage-dependent cardiac Na+ channel,
is an integral membrane protein involved in the initiation and conduction of action potentials …

During the past decade, Nav1. 5, the main voltage-gated Na+ channel in the heart, has been
shown to be involved in many cardiac diseases. Genetic variants in the gene SCN5A …

The cardiac voltage-gated Na+ channel Nav1. 5 generates the cardiac Na+ current (INa).
Mutations in SCN5A, the gene encoding Nav1. 5, have been linked to many cardiac …

The cardiac sodium current (INa) is responsible for the rapid depolarization of cardiac cells,
thus allowing for their contraction. It is also involved in regulating the duration of the cardiac …

Cardiac Diseases Caused by SCN5A Mutations. A prerequisite for a normal cardiac function
is a proper generation and propagation of electrical impulses. Contraction of the heart is …

The cardiac voltage-gated Na+ channel, Na V 1.5, is responsible for the upstroke of the
action potential in cardiomyocytes and for efficient propagation of the electrical impulse in …

The cardiac sodium channel NaV1. 5, encoded by the SCN5A gene, is responsible for the
fast upstroke of the action potential. Mutations in SCN5A may cause sodium channel …

In cardiomyocytes, the rapid depolarisation of the membrane potential is mediated by the α‐
subunit of the cardiac voltage‐gated Na+ channel (NaV1. 5), encoded by the gene SCN5A …

The voltage-gated Na channel isoform 1.5 (NaV1. 5) is the pore forming α-subunit of the
voltage-gated cardiac Na channel, which is responsible for the initiation and propagation of …

The voltage-gated sodium channel 1.5 (Nav1. 5), encoded by the SCN5A gene, is
responsible for the rising phase of the action potential of cardiomyocytes. The sodium …