CACNA1G Membrane Protein Introduction

Introduction of CACNA1G

CACNA1G is a kind of calcium channel, voltage-dependent, T type, alpha 1G subunit, which is also known as CACNA1G or Ca_v3.1, that in humans is encoded by the CACNA1G gene. The calcium influx caused by low-voltage-activated calcium channels is transient (owing to fast inactivation) and tiny (owing to small conductance), so it is identified as 'T' type channels. T-type channels are involved in a variety of pacemaker activities including low-threshold calcium spikes, neuronal oscillations, as well as resonance, and rebound burst firing.

Function ofCACNA1G Membrane Protein

CACNA1G is a calcium channel, which is voltage-dependent, L-type calcium channel subunit alpha-1G. Voltage-sensitive calcium channels (VSCC) are found to show the function of mediating 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-1G is able to cause T-type calcium currents. T-type calcium channels belong to the "low-voltage activated (LVA)" group and are strongly blocked by mibefradil. A particularity of this type of channel is an opening at quite negative potentials and a voltage-dependent inactivation. T-type channels serve pacemaking functions in both central neurons and cardiac nodal cells and support calcium signaling in secretory cells and vascular smooth muscle. They also have been found to be involved in the regulation of firing patterns of neurons which is critical for information processing as well as in cell growth processes.

Fig.1 A topological map of CACNA1G variants (Ha, 2017)

Application of CACNA1G Membrane Protein in Literature

1. Li Y. Long non-coding RNA CACNA1G-AS1 promotes calcium channel protein expression and positively affects human keloid fibroblast migration. Oncol Lett. 2018, 16(1): 891-897. PubMed ID: 29963160
   
   

   This article shows that the long non-coding RNA CACNA1G-AS1 (CAS1) can promote calcium channel protein and type I collagen expression, and have a positive effect on cell migration in human keloid fibroblasts. Therefore, it has been potentially regarded as a novel therapeutic target for keloids.

2. Chemin J., et al. De novo mutation screening in childhood-onset cerebellar atrophy identifies gain-of-function mutations in the CACNA1G calcium channel gene. Brain. 2018, 141(7): 1998-2013. PubMed ID: 29878067
   
   

   This article highlights the prevalence of de novo mutations in early-onset cerebellar atrophy and demonstrates that A961T and M1531V are gain of function mutations. Moreover, it reveals that aberrant activity of Ca_v3.1 channel can markedly alter brain development and suggests that this condition could be amenable to treatment.

3. Yu P.F., et al. Long non-coding RNA CACNA1G-AS1 promotes cell migration, invasion and epithelial-mesenchymal transition by HNRNPA2B1 in non-small cell lung cancer. Eur Rev Med Pharmacol Sci. 2018, 22(4): 993-1002. PubMed ID: 29509247
   
   

   This study finds that CACNA1G-AS1 is identified as an oncogene in NSCLC for the first time, and could promote cell invasion, migration and EMT via increasing HNRNPA2B1 expression, providing a novel target for the biological therapy and prevention.

4. Chemin J., et al. Calmodulin regulates Ca_v3 T-type channels at their gating brake. J Biol Chem. 2017, 292(49): 20010-20031. PubMed ID: 28972185
   
   

   This article concludes that the presence of high-nanomolar affinity binding sites for CaM at its universal gating brake and its unique form of regulation via the tuning of the voltage range of activity could influence the participation of Ca_v3 T-type channels including Ca_v3.2 in heart and brain rhythms.

5. Ha S.E., et al. Transcriptome analysis of PDGFRα+ cells identifies T-type Ca²⁺ channel CACNA1G as a new pathological marker for PDGFRα+ cell hyperplasia. PLoS One. 2017, 12(8): e0182265. PubMed ID: 28806761
   
   

   This article suggests that Cacna1g is exclusively expressed in serosal PDGFRα+ cells, so it is a new pathological marker for gastrointestinal diseases.

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Reference

1. Ha S E, et al. (2017). Transcriptome analysis of PDGFRα+ cells identifies T-type Ca²⁺ channel CACNA1G as a new pathological marker for PDGFRα+ cell hyperplasia. PLoS One. 12(8): e0182265.

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