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nav1 5 voltage gated sodium channel

Nav1.5 belongs to the family of voltage-gated sodium channels, which permit, under physiological conditions, the sodium influx from the extracellular space into the cytosol after depolarization. The most widely used previous name is SCNA5A and SkM2 sodium channel or tetrodotoxin-resistant Na+ current. This channel type is predominantly expressed in heart muscle cells. This Na+ channel is involved in the generation of action potentials in heart muscle cells and, therefore, also responsible for regular rhythm in the heart. Channel activity is regulated by transmembrane potential. The channels are insensitive to the classical sodium channel blocker tetrodotoxin (TTX), but blocked by local anesthetics (here used as antiarrhythmics). Like the other TTX-resistant Na+ channels, its gene is localized on the Chromosome 3 (Human) in contrast to the TTX-sensitive Na+ channel on Chromosome 2. Sodium channels are transmembrane voltage-dependent proteins responsible for the depolarizing phase of the action potential in most electrically excitable cells. They may exist in 3 states: the resting state, where the channel is closed; the activated state, where the channel is open; and the inactivated state, where the channel pore is open but does not conduct ions. The structure of Nav1.5 is based on 4 internal repeats of a 6-helix bundle (in which 5 of the membrane-spanning segments are hydrophobic and the other is positively charged), forming a 24-helical bundle. The charged segments are believed to be localized within clusters formed by their 5 hydrophobic neighbors: it is postulated that the charged domain may be the voltage sensor region, possibly moving outward on depolarization, causing a conformational change. Some heart diseases, such as the long QT syndrome, could be linked to mutations of the gene of the Nav1.5 channel. Also, a slow-down of conduction velocity and ventricular tachycardia were observed after targeted disruption of the cardiac sodium channel gene Scn5a …