CACNA1E Membrane Protein Introduction

Introduction of CACNA1E

CACNA1E, Calcium channel, voltage-dependent, R-type calcium channel subunit alpha-1E (also known as Ca_v2.3) is a protein that in humans is encoded by the CACNA1E gene. The α1 subunit forms the pore through which calcium enters the cell and determines most properties of the channel. It’s strongly expressed in cortex, hippocampus, striatum, amygdala and interpeduncular nucleus, and has a high threshold of activation and relatively slow kinetics.

Function of CACNA1E Membrane Protein

CACNA1E is a voltage-dependent, R-type calcium channel subunit alpha-1E. Voltage-sensitive calcium channels (VSCC) mediate the entry of calcium ions into excitable cells and are also involved in a variety of calcium-dependent processes, including muscle contraction, gene expression, hormone or neurotransmitter release, cell motility, as well as cell division and cell death. The isoform alpha-1E will cause R-type calcium currents. R-type calcium channels are members of the 'high-voltage activated' (HVA) group and are blocked by nickel, and partially blocked by omega-agatoxin-IIIA (omega-Aga-IIIA). CACNA1E is insensitive to omega-conotoxin-GVIA (omega-CTx-GVIA), and omega-agatoxin-IVA (omega-Aga-IVA), as well as dihydropyridines (DHP). Calcium channels containing alpha-1E subunit also have been reported to be involved in the regulation of firing patterns of neurons which are necessary for information processing.

Fig.1 Transmembrane topology of the Ca_v2.3. (Parajuli, 2012)

Application of CACNA1E Membrane Protein in Literature

1. Gandla J., et al. miR-34c-5p functions as pronociceptive microRNA in cancer pain by targeting Ca_v2.3 containing calcium channels. Pain. 2017, 158(9): 1765-1779. PubMed ID: 28614186
   
   

   This article shows that Ca_v2.3 is a new mechanistic target for a key pronociceptive miRNA, miR-34c-5p, in the context of cancer pain and indicates an antinociceptive role for Ca_v2.3 in peripheral sensory neurons. The current study provides a good understanding of molecular mechanisms underlying cancer pain and suggests a potential novel therapeutic strategy targeting miR-34c-5p and Ca_v2.3 in cancer pain.

2. Ambrosini A., et al. Possible Involvement of the CACNA1E Gene in Migraine: A Search for Single Nucleotide Polymorphism in Different Clinical Phenotypes. Headache. 2017, 57(7): 1136-1144. PubMed ID: 28573794
   
   

   This article is to search for differences in the prevalence of a CACNA1E variant between a migraine without aura, various phenotypes of a migraine with aura, and healthy controls, and shows that the missense variant might modulate the function of R-type Ca²⁺ channels.

3. Amano K., et al. Opposite Associations Between the rs3845446 Single-Nucleotide Polymorphism of the CACNA1E Gene and Postoperative Pain-Related Phenotypes in Gastrointestinal Surgery Versus Previously Reported Orthognathic Surgery. J Pain. 2016, 17(10): 1126-1134. PubMed ID: 27480382
   
   

   This study suggests that pain-related phenotypes after gastrointestinal surgery are enhanced in carriers of the minor G allele of the rs3845446 SNP, possibly through impairment of Ca_v2.3 VACC function that is responsible for the activation of visceral inflammatory pain stimulus-elicited antinociception.

4. Wang K., et al. Apamin Boosting of Synaptic Potentials in Ca_v2.3 R-Type Ca²⁺ Channel Null Mice. PLoS One. 2015, 10(9): e0139332. PubMed ID: 26418566
   
   

   This article indicates that SK2-containing channels are functionally coupled to NMDARs and KV4.2-containing channels to Ca_v2.3 channels to provide negative feedback regulation of EPSPs in the spines of CA1 pyramidal neurons.

5. Drobinskaya I., et al. Diethyldithiocarbamate-mediated zinc ion chelation reveals role of Ca_v2.3 channels in glucagon secretion. Biochim Biophys Acta. 2015, 1853(5): 953-64. PubMed ID: 25603538
   
   

   This article indicates that Ca_v2.3 channel is critically involved in the Zn²⁺-mediated suppression of glucagon secretion during hyperglycemia. Especially under conditions of Zn²⁺ deficiency, ablation or dysfunction of Ca_v2.3 channels may lead to severe disturbances in glucose homeostasis.

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Reference

1. Parajuli L K, et al. (2012). Quantitative regional and ultrastructural localization of the Ca(v)2.3 subunit of R-type calcium channel in mouse brain. J Neurosci. 32(39): 13555-67.

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