background:
SCN3B is one member of the sodium channel beta subunits of voltage-gated sodium channels, which are responsible for the generation and propagation of action potentials in neurons and muscle. SCN3B influences the inactivation kinetics of the sodium channel.
Function:
Modulates channel gating kinetics. Causes unique persistent sodium currents. Inactivates the sodium channel opening more slowly than the subunit beta-1. Its association with neurofascin may target the sodium channels to the nodes of Ranvier of developing axons and retain these channels at the nodes in mature myelinated axons (By similarity).
Subunit:
The voltage-sensitive sodium channel consists of an ion conducting pore forming alpha-subunit regulated by one or more beta-1, beta-2 and/or beta-3 subunits. Beta-1 and beta-3 are non-covalently associated with alpha, while beta-2 is covalently linked by disulfide bonds. Beta-1 or beta-3 subunits associate with neurofascin. Associates with SCN10A (By similarity).
DISEASE:
Brugada syndrome 7 (BRGDA7) [MIM:613120]: A tachyarrhythmia characterized by right bundle branch block and ST segment elevation on an electrocardiogram (ECG). It can cause the ventricles to beat so fast that the blood is prevented from circulating efficiently in the body. When this situation occurs, the individual will faint and may die in a few minutes if the heart is not reset. Note=The disease is caused by mutations affecting the gene represented in this entry.
Similarity:
Belongs to the sodium channel auxiliary subunit SCN3B (TC 8.A.17) family.
Contains 1 Ig-like C2-type (immunoglobulin-like) domain.
Database links:
UniProtKB/Swiss-Prot: Q9NY72.1
Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
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