Cav2.3 Protein (R Type Calcium Channel Alpha 1E) 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.
Cav2.3 Protein (R Type Calcium Channel Alpha 1E) 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 .infobox-protein
| protein_name = Cav2.3 Protein
| gene = CACNA1E
| uniprot_id = Q15878
| molecular_weight = ~250 kDa
| localization = Neuronal plasma membrane
| family = Voltage-gated calcium channel family
}}
CACNA1E encodes the alpha-1E subunit of R-type voltage-gated calcium channels (Cav2.3).
- 24 transmembrane segments organized in four domains
- S4 voltage sensor segments in each domain
- Multiple regulatory sites for modulation
- R-type calcium current (HVA calcium currents)
- Dendritic calcium influx
- Synaptic plasticity
- Neuronal excitability
- Role in specific neuronal populations (cerebellar Purkinje cells, hippocampal CA1 neurons)
- Altered R-type channel expression in hippocampus
- Contributes to calcium dysregulation in AD neurons
- Modulates excitability of dopaminergic neurons
- May be involved in neurodegeneration susceptibility
- Gain-of-function mutations associated with epileptic encephalopathy
- Role in seizure generation
- R-type calcium channel blockers (e.g., SNX-482, nickel)
- Limited therapeutic agents currently available
- Research ongoing for selective inhibitors
Cav2.3 Protein (R Type Calcium Channel Alpha 1E) 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 Cav2.3 Protein (R Type Calcium Channel Alpha 1E) 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.
- Zamponi GW, Striessnig J, Koschak A, Dolphin AC. The physiology, pathology, and pharmacology of voltage-gated calcium channels and their therapeutic potential. Physiological Reviews. 2015;95(3):751-848. PMID:26269526
- Catterall WA, Perez-Reyes E, Snutch TP, Striessnig J. Voltage-gated calcium channels. Pharmacological Reviews. 2005;57(4):411-425. PMID:16382099
- Dolphin AC. Calcium channel diversity. Neuropharmacology. 2022;210:109028. PMID:35248423
- Simms BA, Zamponi GW. Neuronal voltage-gated calcium channels: structure, function, and dysfunction. Neuron. 2014;81(2):266-277. PMID:24462094
- Nanou E, Catterall WA. Calcium channels, synaptic plasticity, and neuropsychiatric disease. Neuron. 2018;99(5):918-931. PMID:30138589
- F百姓 Y, Lipscombe D. Neuronal calcium channels: splicing for optimal performance. Current Opinion in Neurobiology. 2019;57:33-40. PMID:30665088
- Huang J, Zamponi GW. Targeting voltage-gated calcium channels for neurodegenerative disease. Expert Opinion on Therapeutic Targets. 2017;21(10):987-996. PMID:28854863
- Talley EM, Cribbs LL, Lee JH, et al. Differential distribution of three members of a gene family encoding low voltage-activated (T-type) calcium channels. Journal of Neuroscience. 1999;19(6):1895-1911. PMID:10066243
- [[genes/cacna1e]]
- [[mechanisms/calcium-channel-dysfunction-neurodegeneration]]
- [[mechanisms/calcium-signaling-dysregulation]]