Scn10A Gene is an important component in the neurobiology of neurodegenerative diseases. This page provides detailed information about its structure, function, and role in disease processes.
.infobox .infobox-gene
| Gene Symbol | SCN10A |
|---|---|
| Gene Name | Sodium Voltage-Gated Channel Alpha Subunit 10 |
| Chromosome | 3p21-p22 |
| NCBI Gene ID | 6336 |
| OMIM ID | 613217 |
| Ensembl ID | ENSG00000185313 |
| UniProt ID | Q9Y5Y9 |
| Associated Diseases | Pain Disorders, Small Fiber Neuropathy, Cardiac Arrhythmias, Brugada Syndrome |
| --- | --- |
| Categories | Ion Channels, Pain Signaling, Sodium Channel Biology |
SCN10A (Sodium Voltage-Gated Channel Alpha Subunit 10) encodes the Nav1.8 sodium channel, a voltage-gated sodium channel primarily expressed in peripheral neurons. This channel is crucial for the generation and propagation of action potentials in nociceptive (pain-sensing) neurons and contributes to cardiac electrical conduction [1][2]. SCN10A variants have been associated with increased risk for cardiac arrhythmias, chronic pain disorders, and certain neuropathic conditions, making it an important target for both cardiac and pain therapeutics.
SCN10A encodes Nav1.8, a voltage-gated sodium channel predominantly expressed in peripheral sensory neurons. Nav1.8 is critical for pain signal transmission and is a major target for analgesic drug development[1].
Nav1.8 exhibits unique properties:
Nav1.8 is expressed in:
SCN10A mutations cause small fiber neuropathy characterized by:
SCN10A variants are associated with:
Common variants in SCN10A influence:
Nav1.8 is a prime target for pain therapeutics:
The study of Scn10A Gene 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.
[3] SCN10A cardiac effects (2021)
[4] Nav1.8 therapeutics (2022)