SCN5A

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SCN5A

A gene on chromosome 3p21 that encodes an integral membrane protein and tetrodotoxin-resistant voltage-gated sodium channel alpha subunit, which is expressed primarily in cardiac myocytes and is responsible beginning the action potential as seen on an ECG/EKG.
 
Molecular pathology
SCN5A mutations are long QT syndrome type 3.
References in periodicals archive ?
Leffler, "Inhibition of the cardiac Na+ channel a-subunit Nav1.5 by propofol and dexmedetomidine," Naunyn-Schmiedeberg's Archives of Pharmacology, vol.
Although inhibition of the hERG channel (human ether-a-go-go-related gene) regulating the major repolarizing current in the heart, IKr (delayed inward potassium current), is the most common mechanism of QT prolongation [4, 5], it can also be caused by the drug triggered inhibition of other channels, that is, potassium (Kv7.1), sodium (Nav1.5), or calcium (Cav1.2) [6-9].
Recent studies have demonstrated that multiple miRs are involved in the regulation of SCN5A/ Nav1.5 channel and its [beta]1/SCN1B subunit which is responsible for the fast-activating, fast-inactivating sodium current in atrial and ventricular action potentials [88].
Guerrero-Serna et al., "Nav1.5 N-terminal domain binding to a1-syntrophin increases membrane density of human Kir2.1, Kir2.2 and Nav1.5 channels," Cardiovascular Research, vol.
BPA can bind directly to and block the Nav1.5 sodium channel (O'Reilly et al.
This defect causes patients to have a disruption in bowel function, by affecting the Nav1.5 channel, a sodium channel in the gastrointestinal smooth muscle and pacemaker cells.
Carrithers, "The human macrophage sodium channel NaV1.5 regulates mycobacteria processing through organelle polarization and localized calcium oscillations," FEMS Immunology and Medical Microbiology, vol.
Chihara, "Fibrillation potentials of denervated rat skeletal muscle are associated with expression of cardiac-type voltage-gated sodium channel isoform Nav1.5," Clinical Neurophysiology, vol.
The Nav1.5 a subunit is the principal component of INa channel forming the pore and all essential gating elements, which is sufficient by itself for generating INa in heterologous expression systems.
For example, Nav1.6 is the variety present at the nodes of Ranvier, Nav1.5 is in the heart muscle, and others such as Navl.7, Nav1.8 and Nav1.9 are predominant in pain-sensing neurons.
Long QT3 syndrome results from an increase in sodium channel function due to mutation in a protein Nav1.5 coded by the gene SCN5A.
Liang, "Solution structure of Jingzhaotoxin-III, a peptide toxin inhibiting both Nav1.5 and Kv2.1 channels," Toxicon, vol.