Introduction of CACNA1G
CACNA1G is a kind of calcium channel, voltage-dependent, T type, alpha 1G subunit, which is also known as CACNA1G or Cav3.1, 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.
|Basic Information of CACNA1G|
|Protein Name||Voltage-dependent T-type calcium channel subunit alpha-1G|
|Aliases||Cav3.1c, NBR13, Voltage-gated calcium channel subunit alpha Cav3.1, KIAA1123|
|Organism||Homo sapiens (Human)|
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
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.
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 Cav3.1 channel can markedly alter brain development and suggests that this condition could be amenable to treatment.
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.
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 Cav3 T-type channels including Cav3.2 in heart and brain rhythms.
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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