CACNA1I Membrane Protein Introduction

Introduction of CACNA1I

CACNA1I, calcium channel, voltage-dependent, T type, alpha 1I subunit, also known as CACNA1I or Ca_v3.3, is a protein which in humans is encoded by the CACNA1I gene. This kind of voltage-sensitive calcium channel mediates the calcium influx into excitable cells and is also involved in a variety of calcium-dependent processes, such as muscle contraction, neurotransmitter release or hormone, gene expression, cell division, motility, and death. A special characteristic of this type of channels is an opening at quite negative potentials.

Function ofCACNA1I Membrane Protein

CACNA1I is also called Ca_v3.3. Mediating the calcium influx into excitable cells, this kind of voltage-sensitive calcium channel is also involved in a variety of calcium-dependent processes, such as muscle contraction, neurotransmitter release or hormone, gene expression, cell division, motility, and death. A special characteristic of this type of channels is an opening at quite negative potentials. It belongs to the "low-voltage activated" group and can be strongly blocked by mibefradil and nickel. In addition, it serves pacemaking functions in both central neurons and cardiac nodal cells and supports calcium signaling in secretory cells and vascular smooth muscle. It also may be involved in the modulation of firing patterns of neurons which is vital for information processing and in cell growth processes.

Fig.1 Calcium channel α1 subunit. (Huang, 2017)

Application of CACNA1I Membrane Protein in Literature

1. Sanchez-Sandoval A.L. Contribution of S4 segments and S4-S5 linkers to the low-voltage activation properties of T-type Ca_v3.3 channels. PLoS One. 2018, 13(2): e0193490. PubMed ID: 29474447
   
   

   This article indicates that mutagenesis in the Ca_v3.3 channel has a partial contribution of the S4-S5 linker of Domain II to LVA behavior, with synergic effects observed in double and triple mutations. These findings demonstrate that IIS4 and, IVS4, voltage sensors are important in determining the LVA properties of Ca_v3.3 channels, although the accomplishment of this function relies on the participation of other structural elements such as S4-S5 linkers.

2. Xie Y., et al. Further evidence for the genetic association between CACNA1I and schizophrenia. Hereditas. 2018, 155: 16. PubMed ID: 29308060
   
   

   This article indicates that CACNA1I is a risk gene for schizophrenia in Chinese population. This gene provides further evidence which supports the role of neuronal calcium signaling in SCZ.

3. Xu W., et al. Genetic risk between the CACNA1I gene and schizophrenia in Chinese Uygur population. Hereditas. 2017, 155: 5. PubMed ID: 28725167
   
   

   This study reveals the evidence that important association exists between the CACNA1I gene and schizophrenia in the Uighur Chinese population. Then the study provides functional analysis and genetic association studies to extend this research.

4. Lee N., et al. Ca²⁺ Regulation of Ca_v3.3 T-type Ca²⁺ Channel Is Mediated by Calmodulin. Mol Pharmacol. 2017, 92(3): 347-357. PubMed ID: 28696213
   
   

   This article demonstrates that Ca_v3.3 calcium channel is regulated by intracellular calcium through interaction between Calcium/Calmodulin with the carboxyl terminus of Ca_v3.3.

5. Lu J.M., et al. Neuritin Enhances Synaptic Transmission in Medial Prefrontal Cortex in Mice by Increasing Ca_v3.3 Surface Expression. Cereb Cortex. 2017, 27(7): 3842-3855. PubMed ID: 28475719
   
   

   This article reveals a novel mechanism of neuritin in synaptic transmission in the medial prefrontal cortex, which is by increasing Ca_v3.3 surface expression. This study indicates the IR and ERK signaling pathway is involved in this mechanism.

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Reference

1. Huang H, et al. (2017). Cardiac voltage-gated ion channels in safety pharmacology: Review of the landscape leading to the CiPA initiative. J Pharmacol Toxicol Methods. 87: 11-23.

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