Voltage-dependent T-type calcium channel subunit alpha-1 (CACNA1G (for the alpha-1G isoform, Ca_v_3.1 is also common))

The Voltage-dependent T-type calcium channel subunit alpha-1 is the principal pore-forming protein of a family of low-voltage activated calcium channels (T-type), encoded in humans by several genes including CACNA1G (alpha-1G isoform). These channels facilitate brief, small-amplitude calcium currents that open near the resting membrane potential and inactivate rapidly. They are crucial for pacemaker activity in neurons and cardiac nodal cells, regulation of membrane potential, exocytosis, and synaptic transmission. T-type calcium channels are strongly inhibited by mibefradil, and their dysfunction is linked to epilepsy, cardiac arrhythmias, pain syndromes, and certain neuropsychiatric diseases[1][3][4]. If specificity is desired (alpha-1G, alpha-1H, alpha-1I), the name and abbreviation may be clarified (e.g., Voltage-dependent T-type calcium channel subunit alpha-1G [CACNA1G], alpha-1H [CACNA1H])[1][4].

Other names

T-type calcium channel alpha-1 subunitCav3.1 (alpha-1G)CACNA1G (gene alias)T-type channel alpha-1GTransient calcium channelLow-voltage activated calcium channel alpha-1 subunit

Channel inhibition (direct blockade reduces calcium entry, stabilizes membrane potential, and reduces excitability) Modulation of channel kinetics (some drugs shift activation/inactivation thresholds) Pacemaker suppression (in cardiac or neuronal tissues) Reduction of neurotransmitter/hormone release (via exocytosis inhibition)