CACNA1G

Voltage-sensitive calcium channels mediate the entry of calcium ions into excitable cells, and are also involved in a variety of calcium-dependent processes, including muscle contraction, hormone or neurotransmitter release, gene expression, cell motility, cell division, and cell death. This gene encodes a T-type, low-voltage activated calcium channel. The T-type channels generate currents that are both transient, owing to fast inactivation, and tiny, owing to small conductance. T-type channels are thought to be involved in pacemaker activity, low-threshold calcium spikes, neuronal oscillations and resonance, and rebound burst firing. Many alternatively spliced transcript variants encoding different isoforms have been described for this gene. [provided by RefSeq, Sep 2011]

Calcium Voltage-Gated Channel Subunit Alpha1 G

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, hormone or neurotransmitter release, gene expression, cell motility, cell division and cell death. The isoform alpha-1G gives rise to 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 may also be involved in the modulation of firing patterns of neurons which is important for information processing as well as in cell growth processes.

AV node cell action potential Source: BHF-UCL
AV node cell to bundle of His cell signaling Source: BHF-UCL
Calcium ion import Source: BHF-UCL
Calcium ion transmembrane transport Source: UniProtKB
Cardiac muscle cell action potential involved in contraction Source: BHF-UCL
Chemical synaptic transmission Source: Ensembl
Membrane depolarization during action potential Source: GO_Central
Membrane depolarization during AV node cell action potential Source: BHF-UCL
Membrane depolarization during SA node cell action potential Source: BHF-UCL
Neuronal action potential Source: GO_Central
Positive regulation of calcium ion-dependent exocytosis Source: GO_Central
Regulation of atrial cardiac muscle cell membrane depolarization Source: Ensembl
Regulation of heart rate by cardiac conduction Source: BHF-UCL
Regulation of ion transmembrane transport Source: UniProtKB-KW
Regulation of membrane potential Source: BHF-UCL
Response to nickel cation Source: Ensembl
SA node cell action potential Source: BHF-UCL
SA node cell to atrial cardiac muscle cell signaling Source: BHF-UCL
Sinoatrial node development Source: BHF-UCL

Cytoplasm; Cell membrane

Spinocerebellar ataxia 42 (SCA42): A form of spinocerebellar ataxia, a clinically and genetically heterogeneous group of cerebellar disorders. Patients show progressive incoordination of gait and often poor coordination of hands, speech and eye movements, due to degeneration of the cerebellum with variable involvement of the brainstem and spinal cord. SCA42 is a slowly progressive, autosomal dominant form with variable severity.
Spinocerebellar ataxia 42, early-onset, severe, with neurodevelopmental deficits (SCA42ND): A form of spinocerebellar ataxia, a clinically and genetically heterogeneous group of cerebellar disorders. Patients show progressive incoordination of gait and often poor coordination of hands, speech and eye movements, due to degeneration of the cerebellum with variable involvement of the brainstem and spinal cord. SCA42ND is an early-onset, severe form associated with motor and cognitive impairment, cerebellar atrophy as well as variable features such as facial dysmorphisms, digital anomalies, microcephaly and epilepsy. SCA42ND inheritance is autosomal dominant.

Cytoplasmic: 1-80 aa
Helical: 81-101 aa
Extracellular: 102-119 aa
Helical: 120-141 aa
Cytoplasmic: 142-150 aa
Helical: 151-170 aa
Extracellular: 171-175 aa
Helical: 176-193 aa
Cytoplasmic: 194-213 aa
Helical: 214-234 aa
Extracellular: 235-370 aa
Helical: 371-395 aa
Cytoplasmic: 396-743 aa
Helical: 744-764 aa
Extracellular: 765-777 aa
Helical: 778-799 aa
Cytoplasmic: 800-805 aa
Helical: 806-824 aa
Extracellular: 825-832 aa
Helical: 833-856 aa
Cytoplasmic: 857-867 aa
Helical: 868-888 aa
Extracellular: 889-939 aa
Helical: 940-964 aa
Cytoplasmic: 965-1272 aa
Helical: 1273-1295 aa
Extracellular: 1296-1313 aa
Helical: 1314-1334 aa
Cytoplasmic: 1335-1344 aa
Helical: 1345-1364 aa
Extracellular: 1365-1378 aa
Helical: 1379-1400 aa
Cytoplasmic: 1401-1410 aa
Helical: 1411-1434 aa
Extracellular: 1435-1511 aa
Helical: 1512-1537 aa
Cytoplasmic: 1538-1610 aa
Helical: 1611-1631 aa
Extracellular: 1632-1645 aa
Helical: 1646-1667 aa
Cytoplasmic: 1668-1674 aa
Helical: 1675-1693 aa
Extracellular: 1694-1707 aa
Helical: 1708-1731 aa
Cytoplasmic: 1732-1745 aa
Helical: 1746-1766 aa
Extracellular: 1767-1826 aa
Helical: 1827-1854 aa
Cytoplasmic: 1855-2377 aa

In response to raising of intracellular calcium, the T-type channels are activated by CaM-kinase II.