Voltage-dependent T-type calcium channel subunit alpha-1G
Also known as: CACNA1G, KIAA1123
Function
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.
Classification
- Family (Pfam)
- PF00520 Ion_trans
- InterPro
- Ion_trans_dom, VDCC_alpha-1_subunit, VDCC_T_a1, VDCCAlpha1, Volt_channel_dom_sf
- Functional cluster
- Homeobox & Zinc-Finger Transcription Factors
Experimental structures · PDB · 2
A predicted model is available from AlphaFold.
Gene Ontology · 22
- GO:0005737 cytoplasm
- GO:0005886 plasma membrane
- GO:0005891 voltage-gated calcium channel complex
- GO:0008331 high voltage-gated calcium channel activity
- GO:0008332 low voltage-gated calcium channel activity
- GO:0097110 scaffold protein binding
- GO:0005245 voltage-gated calcium channel activity
- GO:0086056 voltage-gated calcium channel activity involved in AV node cell action potential
- GO:0086059 voltage-gated calcium channel activity involved SA node cell action potential
- GO:0086016 AV node cell action potential
- GO:0086027 AV node cell to bundle of His cell signaling
- GO:0070509 calcium ion import
- GO:0098703 calcium ion import across plasma membrane
- GO:0070588 calcium ion transmembrane transport
- GO:0086002 cardiac muscle cell action potential involved in contraction
- GO:0086045 membrane depolarization during AV node cell action potential
- GO:0086046 membrane depolarization during SA node cell action potential
- GO:0086091 regulation of heart rate by cardiac conduction
- GO:0042391 regulation of membrane potential
- GO:0086015 SA node cell action potential
- GO:0086018 SA node cell to atrial cardiac muscle cell signaling
- GO:0003163 sinoatrial node development
Disease associations
- spinocerebellar ataxia type 42 MONDO:0014776
- spinocerebellar ataxia 42, early-onset, severe, with neurodevelopmental deficits MONDO:0060758
Drugs targeting this protein · 17
- PREGABALIN modulator
- PARAMETHADIONE blocker
- BEPRIDIL HYDROCHLORIDE blocker
- MIBEFRADIL DIHYDROCHLORIDE blocker
- GABAPENTIN ENACARBIL modulator
- SUVECALTAMIDE modulator
- IMAGABALIN modulator
- SULOCTIDIL blocker
- APINOCALTAMIDE blocker
- PHLOROGLUCINOL blocker
- TERODILINE HYDROCHLORIDE blocker
- ATAGABALIN modulator
- TRIMETHADIONE blocker
- ETHOSUXIMIDE blocker
- METHSUXIMIDE blocker
- PHENSUXIMIDE blocker
- GABAPENTIN modulator
Related proteins · sequence + function similarity
- Voltage-dependent T-type calcium channel subunit alpha-1G 0.99
- Voltage-dependent T-type calcium channel subunit alpha-1H 0.95
- Voltage-dependent T-type calcium channel subunit alpha-1H 0.94
- Voltage-dependent T-type calcium channel subunit alpha-1I 0.94
- Voltage-dependent T-type calcium channel subunit alpha-1I 0.94
- Voltage-dependent T-type calcium channel subunit alpha-1H 0.93
- Voltage-dependent L-type calcium channel subunit alpha-1F 0.88
- Voltage-dependent L-type calcium channel subunit alpha-1F 0.88
- Sodium channel protein type 5 subunit alpha 0.81
- Sodium channel protein type 5 subunit alpha 0.81
- Sodium channel protein type 10 subunit alpha 0.80
- Sodium channel protein type 10 subunit alpha 0.79
Co-cited proteins · studied together in the literature
- Voltage-dependent T-type calcium channel subunit alpha-1G 1 shared papers
Literature · 13 cited papers
- De novo mutation screening in childhood-onset cerebellar atrophy identifies gain-of-function mutations in the CACNA1G calcium channel gene. Brain · 2018
- A mutation in the low voltage-gated calcium channel CACNA1G alters the physiological properties of the channel, causing spinocerebellar ataxia. Mol. Brain · 2015
- A recurrent mutation in CACNA1G alters Cav3.1 T-type calcium-channel conduction and causes autosomal-dominant cerebellar ataxia. Am. J. Hum. Genet. · 2015
- Profiling the array of Ca(v)3.1 variants from the human T-type calcium channel gene CACNA1G: alternative structures, developmental expression, and biophysical variations. Proteins · 2006
- DNA sequence of human chromosome 17 and analysis of rearrangement in the human lineage. Nature · 2006
- The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC). Genome Res. · 2004
- Construction of expression-ready cDNA clones for KIAA genes: manual curation of 330 KIAA cDNA clones. DNA Res. · 2002
- Molecular and functional properties of the human alpha1G subunit that forms T-type calcium channels. J. Biol. Chem. · 2000
- Molecular cloning and functional expression of ca(v)3.1c, a T-type calcium channel from human brain. FEBS Lett. · 2000
- Characterization of cDNA clones selected by the GeneMark analysis from size-fractionated cDNA libraries from human brain. DNA Res. · 1999
- Structure and alternative splicing of the gene encoding alpha1G, a human brain T calcium channel alpha1 subunit. Neurosci. Lett. · 1999
- Inactivation of CACNA1G, a T-type calcium channel gene, by aberrant methylation of its 5' CpG island in human tumors. Cancer Res. · 1999
- … and 1 more in the literature graph