Cav3.2 Protein (T Type Calcium Channel Alpha 1H) 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.
Cav3.2 Protein (T Type Calcium Channel Alpha 1H) 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 = Cav3.2 Protein
| gene = CACNA1H
| uniprot_id = O43496
| molecular_weight = ~250 kDa
| localization = Neuronal plasma membrane, dendrites
| family = T-type calcium channel family
}}
CACNA1H encodes the alpha-1H subunit of low-voltage-activated T-type calcium channels (Cav3.2).
- 24 transmembrane segments in four domains
- Unique voltage dependence among T-type channels
- Multiple splice variants
- Low-threshold calcium influx
- Neuronal pacemaking
- Thalamic burst firing
- Regulation of sleep-wake cycles
- Dendritic integration
- Upregulated in AD brain
- Contributes to neuronal hyper excitability
- May promote calcium dysregulation
- Multiple mutations cause childhood absence epilepsy
- Enhanced T-type currents lead to absence seizures
- Upregulated in dorsal horn neurons
- Contributes to pain sensitization
- Ethosuximide (first-line for absence seizures)
- Zonisamide
- T-type selective blockers in development
- Anti-epileptic drugs acting on T-type channels
Cav3.2 Protein (T Type Calcium Channel Alpha 1H) 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 Cav3.2 Protein (T Type Calcium Channel Alpha 1H) 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/cacna1h]]
- [[mechanisms/calcium-channel-dysfunction-neurodegeneration]]
- [[mechanisms/calcium-signaling-dysregulation]]