Nav1.5 Sodium Channel is an important component in the neurobiology of neurodegenerative diseases. This page provides detailed information about its structure, function, and role in disease processes.
Nav1.5 (SCN5A) is the principal cardiac sodium channel responsible for the rapid depolarization of cardiac myocytes. It is critical for cardiac conduction and rhythm.
This protein is involved in:
- Cardiac depolarization: Mediates rapid Na+ influx in heart
- Conduction: Enables impulse propagation through cardiac tissue
- Heart rhythm: Maintains normal cardiac rhythm
| Attribute |
Value |
| Protein Name |
Nav1.5 |
| Gene |
SCN5A |
| UniProt ID |
Q14524 |
| PDB IDs |
6L2J, 7JX2 |
| Molecular Weight |
~260 kDa |
| Subcellular Localization |
Cardiac sarcolemma |
| Protein Family |
Voltage-gated sodium channel (NaV) family |
Nav1.5 shares the canonical sodium channel structure:
- 4 Homologous Domains: Each with 6 transmembrane segments
- Voltage Sensors: Four S4 helices with gating charges
- Pore Domain: Forms ion selectivity filter
- Fast Inactivation Gate: Between DIII and DIV
- C-terminal interactions: With anchoring proteins
- Cardiac Action Potential: Mediates rapid depolarization (Phase 0)
- Conduction: Enables fast impulse propagation
- Excitability: Sets threshold for cardiac activation
- Mechanism: Gain-of-function increases late Na+ current
- Arrhythmia Risk: Torsades de pointes
- Treatment: β-blockers, mexiletine
- Mechanism: Loss-of-function reduces Na+ current
- Sudden Death: Ventricular fibrillation risk
- Treatment: ICD implantation
- Progressive: Age-dependent slowing of conduction
- Pacemaker: Often requires pacemaker implantation
- SCN5A in cardiac disease - Remme CA, et al. Cardiovasc Res 2006 PMID:16448639
The study of Nav1.5 Sodium Channel has evolved significantly over the past decades. Research in this area has revealed important insights into the underlying mechanisms of neurodegeneration and continues to drive therapeutic development.
Historical context and key discoveries in this field have shaped our current understanding and will continue to guide future research directions.
- Gene expression and function in neuronal tissues. PubMed.
- Role in neuronal excitability and synaptic transmission. PubMed.
- Calcium channel dysfunction in neurological disorders. PubMed.
- Voltage-gated ion channels in neurodegeneration. PubMed.