Nutrition Guide

Sodium channel, nonvoltage-gated 1, delta, also known as SCNN1D, is a human gene.

Sodium channel, nonvoltage-gated 1, beta (Liddle syndrome), also known as SCNN1B, is a human gene.[1]

Sodium channel, nonvoltage-gated 1 alpha, also known as SCNN1A, is a human gene.

Sodium channel, voltage gated, type VIII, alpha subunit (SCN8A) is a human gene encoding the Nav1.6 protein.[1]

Sodium channel, voltage-gated, type VII, alpha, also known as SCN7A, is a human gene.[1]

SCN4B is a sodium channel associated with long QT syndrome.

Sodium channel, voltage-gated, type III, beta, also known as SCN3B, is a human gene.[1]

Voltage-gated sodium channels are transmembrane glycoprotein complexes composed of a large alpha subunit and one or more regulatory beta subunits. They are responsible for the generation and propagation of action potentials in neurons and muscle. This gene encodes one member of the sodium channel beta subunit gene family, and influences the inactivation kinetics of the sodium channel. Two alternatively spliced variants, encoding the same protein, have been identified.

Sodium channel, voltage-gated, type III, alpha subunit (SCN3A) is a human gene encoding the Nav1.3 protein,.[1]

Voltage-gated sodium channels are transmembrane glycoprotein complexes composed of a large alpha subunit with 24 transmembrane domains and one or more regulatory beta subunits. They are responsible for the generation and propagation of action potentials in neurons and muscle. This gene encodes one member of the sodium channel alpha subunit gene family, and is found in a cluster of five alpha subunit genes on chromosome 2. Multiple transcript variants encoding different isoforms have been found for this gene.

Sodium channel, voltage-gated, type II, beta, also known as SCN2B, is a human gene.

Sodium channel, voltage-gated, type I, beta, also known as SCN1B, is a human gene.[1]

Voltage-gated sodium channels are essential for the generation and propagation of action potentials in striated muscle and neuronal tissues. Biochemically, they consist of a large alpha subunit and 1 or 2 smaller beta subunits, such as SCN1B. The alpha subunit alone can exhibit all the functional attributes of a voltage-gated Na+ channel, but requires a beta-1 subunit for normal inactivation kinetics.[supplied by OMIM][1]