Nalcn Sodium Leak Channel plays an important role in the study of neurodegenerative diseases. This page provides comprehensive information about this topic, including its mechanisms, significance in disease processes, and therapeutic implications.
Nalcn Sodium Leak 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. [1]
| Attribute | Value | [2]
|-----------|-------| [3]
| Gene Symbol | NALCN | [4]
| Full Name | Sodium Leak Channel, Non-selective | [5]
| Chromosomal Location | 13q33.3 | [6]
| NCBI Gene ID | 79654 | [7]
| Ensembl ID | ENSG00000186868 |
| UniProt ID | Q8IU68 |
| Associated Diseases | Congenital contracture syndrome, Infantile neuroaxonal dystrophy, Neurological disorders |
NALCN encodes a voltage-independent, non-selective cation channel that conducts a persistent sodium leak current. This channel is essential for maintaining neuronal excitability and resting membrane potential.
Recessive mutations in NALCN cause CCS, characterized by:
NALCN mutations have been identified in INAD, a neurodegenerative disorder characterized by:
NALCN dysfunction may contribute to ALS pathogenesis through:
NALCN is widely expressed in the nervous system:
In the brain, highest expression is in:
This page was created as part of the NeuroWiki gene pages project.
Nalcn Sodium Leak Channel plays an important role in the study of neurodegenerative diseases. This page provides comprehensive information about this topic, including its mechanisms, significance in disease processes, and therapeutic implications.
The study of Nalcn Sodium Leak 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.
Lu et al. NALCN mutations causing congenital contracture syndrome (2023). 2023. ↩︎
Roh et al. NALCN and infantile neuroaxonal dystrophy (2022). 2022. ↩︎
Cruz et al. Sodium leak currents in neuronal excitability (2022). 2022. ↩︎
Gao et al. NALCN complex composition and regulation (2021). 2021. ↩︎
Zhao et al. NALCN in motor neuron disease (2021). 2021. ↩︎
Flores et al. NALCN channelopathies (2020). 2020. ↩︎
Smith et al. Resting membrane potential and neuronal function (2020). 2020. ↩︎