Affinage

CACNA1G

Voltage-dependent T-type calcium channel subunit alpha-1G · UniProt O43497

Length
2377 aa
Mass
262.5 kDa
Annotated
2026-04-28
89 papers in source corpus 43 papers cited in narrative 40 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CACNA1G encodes CaV3.1, the pore-forming α1 subunit of a low-voltage-activated (T-type) calcium channel that opens near resting membrane potential to conduct transient inward Ca²⁺ currents critical for rhythmic burst firing, pacemaker depolarization, and subthreshold calcium signaling across diverse excitable and non-excitable cell types. CaV3.1-mediated Ca²⁺ entry drives diastolic depolarization in sinoatrial and atrioventricular node cells for cardiac pacemaking (PMID:16690884), sustains thalamic action-potential silencing required for sleep maintenance (PMID:15677322), supports mGluR1-potentiated dendritic spine Ca²⁺ transients in cerebellar Purkinje cells (PMID:19657020), enables NFAT-dependent GM-CSF production in T helper cells (PMID:27037192), mediates leucine-sensing activation of hypothalamic POMC neurons to suppress appetite (PMID:42025169), and promotes adult hippocampal neurogenesis via CaMKII/Akt/BDNF signaling (PMID:33393208). Channel activity is tuned by extensive alternative splicing that combinatorially adjusts gating (PMID:16671074), post-translational regulation including Cdk5 phosphorylation at Ser2234 (PMID:25760945) and β-adrenergic/PKA-dependent enhancement (PMID:22808078), inhibition by the γ6 subunit through a GxxxA transmembrane motif (PMID:18818244), and transcriptional control by Wnt/LEF1/β-catenin (PMID:20371816) and glucocorticoid/GR/NFκB pathways (PMID:18820838). Gain-of-function missense mutations that impair channel inactivation cause autosomal dominant spinocerebellar ataxia (SCA42) and childhood-onset cerebellar atrophy (PMID:26456284, PMID:29878067), while altered Cacna1g dosage modifies seizure severity in sodium channelopathy models of epilepsy (PMID:27112236).

Mechanistic history

Synthesis pass · year-by-year structured walk · 28 steps
  1. 2003 High

    Defining how extracellular protons and Ca²⁺ interact at the CaV3.1 selectivity filter (EEDD locus) established the biophysical basis of pore selectivity and gating modulation by pH.

    Evidence Pore-locus mutagenesis with pH titration and patch-clamp in HEK293 cells expressing CaV3.1

    PMID:12743167

    Open questions at the time
    • No structural resolution of proton binding sites
    • In vivo relevance of pH modulation not tested
  2. 2003 Medium

    Identification of two functional promoters (A and B) with differentiation-dependent switching explained how CaV3.1 transcription is regulated during neuronal maturation.

    Evidence 5'-RACE, promoter-luciferase reporters in Y79 retinoblastoma cells

    PMID:12752779

    Open questions at the time
    • Promoter switching not validated in primary neurons in vivo
    • Trans-acting factors not identified
  3. 2004 High

    Demonstrating that the γ6 subunit specifically inhibits CaV3.1 current density without altering gating or expression levels revealed a dedicated auxiliary subunit mechanism for T-type channel regulation.

    Evidence Co-expression in HEK-293 and HL-1 atrial cells with patch-clamp and protein quantification

    PMID:15572045

    Open questions at the time
    • Mechanism of current reduction (trafficking vs. gating) not resolved at this stage
    • In vivo significance not tested
  4. 2005 High

    Conditional deletion of Cacna1g from rostral-midline thalamus established that CaV3.1-dependent prolonged firing inhibition is the mechanism by which the thalamus gates arousal signals to stabilize sleep.

    Evidence Cre/loxP conditional KO; patch-clamp with synaptic blockers; polysomnography in mice

    PMID:15677322

    Open questions at the time
    • Downstream Ca²⁺-dependent effectors mediating 9-second firing inhibition not identified
    • Circuit-level mechanism of arousal signal blockade not mapped
  5. 2006 High

    Global Cacna1g knockout abolishing T-type current in SAN/AV node cells and causing bradycardia definitively established CaV3.1 as the molecular basis of T-type current-driven cardiac pacemaking.

    Evidence Cacna1g KO mice; telemetric ECG; patch-clamp of isolated SAN/AV node cells

    PMID:16690884

    Open questions at the time
    • Relative contribution of CaV3.1 vs. HCN channels to pacemaker depolarization under physiological conditions not quantified
    • Compensatory mechanisms in KO not excluded
  6. 2006 High

    Comprehensive transcript profiling revealing 30 splice variants with combinatorial gating effects and developmentally regulated splicing patterns established that alternative splicing is a major mechanism for CaV3.1 functional diversification.

    Evidence Scanning of 1580 full-length cDNAs; patch-clamp of 9 selected variants; 5'-RACE

    PMID:16671074

    Open questions at the time
    • Functional significance of most variant combinations untested
    • Cell-type-specific splice variant expression not mapped
  7. 2006 High

    Chimeric domain-swapping between CaV3.1 and CaV3.3 identified domain IV as the primary determinant of activation kinetics and recovery from inactivation, localizing key gating differences to specific structural modules.

    Evidence Chimeric channel constructs with whole-cell patch-clamp in tsA-201 cells

    PMID:16996222

    Open questions at the time
    • Specific residues within domain IV responsible not identified
    • No structural model available
  8. 2006 High

    Showing that CaV3.1 controls thrombin-induced VWF secretion from pulmonary microvascular endothelial cells extended the channel's functional repertoire beyond excitable cells to regulated exocytosis in endothelium.

    Evidence shRNA knockdown and recombinant CaV3.1 overexpression; GFP-VWF real-time imaging; Ca²⁺ imaging

    PMID:17172292

    Open questions at the time
    • Ca²⁺ microdomain coupling between CaV3.1 and secretory machinery not characterized
    • Relevance to hemostasis in vivo not tested
  9. 2008 High

    Mutational analysis of the γ6 GxxxA transmembrane motif, combined with co-IP in native atrial myocytes, established that helix-helix interactions within the membrane underlie γ6-mediated CaV3.1 inhibition, and a synthetic GxxxA peptide could recapitulate this inhibition.

    Evidence Site-directed mutagenesis; co-IP in HEK cells and atrial myocytes; single-channel and whole-cell patch-clamp; peptide electrophysiology

    PMID:18818244 PMID:19193827

    Open questions at the time
    • Binding interface on CaV3.1 not mapped
    • Stoichiometry of γ6-CaV3.1 complex unknown
  10. 2008 High

    Systematic permeation studies with Ni²⁺, Ca²⁺, Ba²⁺, and surface charge analysis defined the biophysical principles of CaV3.1 ion selectivity and pore block, establishing a quantitative framework for divalent cation interactions at two distinct pore sites.

    Evidence Whole-cell patch-clamp with ion substitution, Woodhull modeling, and Gouy-Chapman-Stern analysis in HEK293 cells

    PMID:18663131 PMID:18663132

    Open questions at the time
    • No atomic-resolution pore structure available
    • Physiological relevance of surface charge effects in native membranes not tested
  11. 2008 High

    Attenuated neuropathic pain in CaV3.1 KO mice after spinal nerve ligation identified the channel as a required contributor to neuropathic pain processing.

    Evidence CaV3.1 KO mice; behavioral pain assays with mechanical and thermal thresholds

    PMID:18414012

    Open questions at the time
    • Spinal vs. supraspinal site of action not determined
    • Downstream signaling from CaV3.1 Ca²⁺ entry to pain sensitization unknown
  12. 2008 Medium

    Identification of functional glucocorticoid response elements in the Cacna1g promoter established a transcriptional mechanism for corticosteroid-mediated upregulation of T-type current in cardiomyocytes.

    Evidence Promoter-luciferase with GRE mutagenesis; GR antagonist; NFκB inhibitor; patch-clamp in neonatal cardiomyocytes

    PMID:18820838 PMID:19705257

    Open questions at the time
    • Direct GR occupancy at endogenous Cacna1g GREs not shown by ChIP
    • Physiological significance of glucocorticoid regulation in adult heart not tested
  13. 2009 High

    Demonstrating mGluR1-dependent potentiation of CaV3.1 in cerebellar Purkinje cell dendritic spines established a T-type channel-mediated fast Ca²⁺ signaling mechanism for synaptic integration of parallel fiber inputs.

    Evidence Whole-cell patch-clamp; ultrafast two-photon Ca²⁺ imaging; immunoelectron microscopy; CaV3.1 KO animals

    PMID:19657020

    Open questions at the time
    • Downstream Ca²⁺ effectors in dendritic spines not identified
    • Behavioral consequence of impaired spine Ca²⁺ signaling not tested
  14. 2010 High

    ChIP demonstrating LEF1/β-catenin binding to the Cacna1g promoter in thalamic neurons in vivo, combined with WNT3A-induced T-type current increases, established Wnt signaling as a transcriptional activator of CaV3.1 in the brain.

    Evidence Chromatin immunoprecipitation; luciferase reporter; DNase I footprinting; patch-clamp of cultured thalamic neurons

    PMID:20371816

    Open questions at the time
    • Whether Wnt-driven CaV3.1 upregulation contributes to thalamic oscillations in vivo not tested
    • Other Wnt target genes acting in parallel not controlled for
  15. 2010 High

    Identification of CaV3.1 as the dominant voltage-gated Ca²⁺ channel in preadipocytes required for cell cycle entry, and its upregulation by IGF-I/PI3K/Akt in pulmonary artery smooth muscle cells linking it to cyclin D expression, established CaV3.1 as a proliferative signal in non-neuronal mitogenic pathways.

    Evidence siRNA/RNAi knockdown; patch-clamp; cell cycle analysis; PI3K/Akt inhibitors in C2C12, primary preadipocytes, and PASMC

    PMID:20457833 PMID:21148410

    Open questions at the time
    • Direct Ca²⁺-dependent mechanism linking channel opening to cyclin D induction not identified
    • In vivo significance for adipogenesis or vascular remodeling not tested
  16. 2012 High

    Quantitative permeation studies showing Fe²⁺ and Cd²⁺ transit through the CaV3.1 pore (with radiolabel confirmation for Cd²⁺) established T-type channels as candidate pathways for toxic and essential divalent metal ion entry into cells.

    Evidence Patch-clamp with Eyring barrier modeling; ¹⁰⁹Cd²⁺ radiolabel uptake in HEK293-CaV3.1 stable cells

    PMID:22973059 PMID:22973060

    Open questions at the time
    • Physiological relevance of Fe²⁺/Cd²⁺ permeation in native tissues not demonstrated
    • Relative contribution vs. dedicated metal transporters unknown
  17. 2012 High

    β-adrenergic/PKA-dependent enhancement of CaV3.1 current in SAN cells identified a neurohumoral mechanism for autonomic modulation of T-type channel activity in cardiac pacemaking.

    Evidence Patch-clamp of CaV3.1 transgenic cardiomyocytes and WT/KO SAN cells; PKA inhibitor H89

    PMID:22808078

    Open questions at the time
    • PKA phosphorylation site on CaV3.1 not identified
    • Contribution to heart rate increase in vivo not quantified
  18. 2012 Medium

    Insulin-stimulated CaV3.1 membrane insertion via Rab11a-dependent endosomal recycling revealed a post-translational trafficking mechanism for acute regulation of T-type current independent of transcription.

    Evidence Patch-clamp; Brefeldin A treatment; dominant-negative Rab11a in HEK-293/CaV3.1 and GH3 pituitary cells

    PMID:22770883

    Open questions at the time
    • Direct visualization of CaV3.1 endosomal trafficking not performed
    • Insulin signaling intermediates connecting to Rab11a not identified
  19. 2015 High

    Identification of CaV3.1 Ser2234 as the Cdk5 phosphorylation site that increases T-type current defined a specific kinase-substrate relationship for post-translational channel modulation in neurons.

    Evidence Site-directed mutagenesis; Cdk5 overexpression/siRNA; patch-clamp in HEK-293 and N1E-115 cells

    PMID:25760945

    Open questions at the time
    • In vivo phosphorylation at Ser2234 not confirmed
    • Downstream physiological consequence of Cdk5-CaV3.1 regulation not established
  20. 2015 High

    The p.Arg1715His mutation in the CaV3.1 S4 voltage sensor shifting activation and inactivation established the first causal link between CACNA1G gain-of-function and autosomal dominant spinocerebellar ataxia (SCA42).

    Evidence Whole-cell patch-clamp of mutant vs. WT in HEK293T; computational modeling; exome sequencing with linkage in families

    PMID:26456284 PMID:26715324

    Open questions at the time
    • Patient-derived neuronal validation not performed at this stage
    • Mechanism of selective cerebellar vulnerability not explained
  21. 2016 High

    CaV3.1 KO mice resisting EAE with reduced T-helper GM-CSF production and impaired NFAT nuclear translocation established an unexpected role for T-type channels in adaptive immune cell activation.

    Evidence CaV3.1 KO mice; EAE model; patch-clamp of T cells; NFAT localization; cytokine assays

    PMID:27037192

    Open questions at the time
    • How resting-potential T-type Ca²⁺ entry triggers NFAT without store depletion is mechanistically unclear
    • Contribution relative to CRAC/Orai channels not quantified
  22. 2016 High

    Bidirectional modification of seizure severity in two sodium channelopathy epilepsy models by Cacna1g dosage established the gene as a genetic modifier operating in epistasis with SCN1A and SCN2A.

    Evidence Transgenic Cacna1g alteration in Scn1a⁺/⁻ and Scn2aQ54 mouse models; seizure and survival monitoring

    PMID:27112236 PMID:28556246

    Open questions at the time
    • Mechanism of T-type/Na⁺ channel epistasis at the circuit level not resolved
    • Human genetic modifier studies not performed
  23. 2018 High

    De novo mutations p.Ala961Thr and p.Met1531Val causing dramatic inactivation impairment and childhood cerebellar atrophy, rescuable by TTA-P2, expanded the genotype-phenotype spectrum and demonstrated pharmacological tractability of CaV3.1 channelopathies.

    Evidence Patch-clamp of transfected cells; TTA-P2 pharmacology; computational cerebellar neuron modeling; whole-exome sequencing

    PMID:29878067

    Open questions at the time
    • In vivo TTA-P2 rescue not attempted
    • Mechanism of selective cerebellar neuron vulnerability still unexplained
  24. 2021 Medium

    CaV3.1 localization to hippocampal neural progenitors and KO-associated deficits in proliferation, differentiation, and BDNF/CaMKII/Akt signaling established the channel as a regulator of adult hippocampal neurogenesis.

    Evidence CaV3.1 KO mice; BrdU labeling; doublecortin immunostaining; Western blot for signaling pathways

    PMID:33393208

    Open questions at the time
    • Causal link between CaV3.1 Ca²⁺ entry and specific downstream kinase activation is correlative
    • Cell-autonomous vs. non-cell-autonomous effects not distinguished
  25. 2022 High

    CaV3.1-driven burst firing in dorsomedial VMH neurons inducing anxiety-like behavior and shifting energy metabolism toward fat oxidation established a defined hypothalamic circuit role for CaV3.1 in stress and metabolism.

    Evidence Optogenetics; Cav3.1 knockdown; respiratory exchange ratio; behavioral assays; in vivo electrophysiology

    PMID:35318460

    Open questions at the time
    • Downstream neuropeptide or neurotransmitter mediators not identified
    • Human relevance not established
  26. 2024 High

    Human thalamocortical assembloids carrying the M1531V GOF variant or CACNA1G KO demonstrated that both gain and loss of CaV3.1 function disrupt thalamocortical connectivity, validating channel-dependent circuit assembly in a human model system.

    Evidence iPSC-derived thalamocortical assembloids; patch-clamp; calcium imaging; axonal projection analysis

    PMID:39419023

    Open questions at the time
    • Whether connectivity defects are reversible with T-type blockers not tested
    • Correlation with patient phenotypes not directly established
  27. 2025 High

    Discovery that leucine directly binds the CaV3.1 voltage-sensing segment to lower activation threshold, activating hypothalamic POMC neurons and suppressing appetite, revealed the channel as a molecular sensor coupling amino acid availability to satiety signaling.

    Evidence Conditional Cacna1g KO in POMC neurons; hypothalamic leucine injection; structural binding analysis; brain slice electrophysiology; diet-induced obesity model

    PMID:42025169

    Open questions at the time
    • Atomic structure of leucine-binding pocket not fully resolved
    • Whether other amino acids share this binding mode unknown
  28. 2025 Medium

    CACNA1G loss-of-function in Xenopus reducing LRO cilia and disrupting left-right patterning revealed an unexpected developmental role for CaV3.1 in ciliogenesis.

    Evidence CRISPR crispants in Xenopus tropicalis; in situ hybridization; LRO cilia morphological analysis

    PMID:40008628

    Open questions at the time
    • Mechanism linking CaV3.1 Ca²⁺ entry to ciliogenesis completely unknown
    • Not confirmed in mammalian systems
    • Channel-independent effects of CRISPR not excluded

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the atomic structure of the CaV3.1 channel, the mechanism by which low-voltage Ca²⁺ entry selectively activates NFAT in T cells, the basis of cerebellar vulnerability in CACNA1G channelopathies, and whether T-type channel blockers can be developed as therapeutics for SCA42 or neurodevelopmental encephalopathies.
  • No high-resolution cryo-EM structure of CaV3.1 reported
  • Therapeutic window for T-type blockers in channelopathies not established
  • Cell-type-specific splice variant functions largely unmapped

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005215 transporter activity 8 GO:0140299 molecular sensor activity 1
Localization
GO:0005886 plasma membrane 6
Pathway
R-HSA-162582 Signal Transduction 5 R-HSA-112316 Neuronal System 4 R-HSA-382551 Transport of small molecules 4 R-HSA-168256 Immune System 1
Partners
CACNG6CDK5GRM1LEF1RAB11A

Evidence

Reading pass · 40 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2006 Genetic knockout of CaV3.1/alpha1G (cacna1g) abolishes T-type calcium current in sinoatrial node (SAN) and atrioventricular node cells, causing bradycardia, delayed AV conduction, prolonged SAN recovery time, and slowed pacemaker activity through reduction of diastolic depolarization slope, without affecting L-type Ca2+ current or right atrial excitability. Cacna1g knockout mice; telemetric ECG; intracardiac recordings; patch-clamp of isolated SAN/AV node cells Circulation Research High 16690884
2005 Thalamic CaV3.1 T-type Ca2+ channel activation causes prolonged inhibition (>9 s) of action-potential firing in thalamic projection neurons via intracellular Ca2+ increase (independent of synaptic transmission), and focal Cre/loxP deletion of Cacna1g from the rostral-midline thalamus fragments and reduces sleep by preventing blockade of arousal signal transmission through the thalamus. CaV3.1 knockout mice; Cre/loxP conditional deletion; patch-clamp with synaptic blockers; polysomnography PNAS High 15677322
2009 mGluR1 activation potentiates CaV3.1 T-type currents in cerebellar Purkinje cell dendritic spines via a G-protein- and tyrosine-phosphatase-dependent pathway; CaV3.1 channels co-localize with mGluR1 in dendritic spines and mediate fast subthreshold Ca2+ signaling potentiated during bursts of parallel fiber inputs. Whole-cell patch-clamp; ultrafast two-photon Ca2+ imaging; immunoelectron microscopy; CaV3.1 knockout animals Journal of Neuroscience High 19657020
2015 The recurrent p.Arg1715His mutation in the S4 voltage sensor of CaV3.1 causes autosomal dominant cerebellar ataxia (SCA42) by positively shifting the current-voltage and steady-state activation curves and increasing the slope factor of inactivation, resulting in decreased neuronal excitability in deep cerebellar nuclei neurons per computational modeling. Whole-cell patch-clamp in HEK293T cells expressing mutant vs. WT CaV3.1; computational neuronal modeling; exome sequencing with linkage analysis American Journal of Human Genetics High 26456284 26715324
2018 De novo gain-of-function mutations p.Ala961Thr and p.Met1531Val in CaV3.1 drastically impair channel inactivation (approximately 5× slower kinetics, >10 mV negative shift of half-inactivation), increase neuronal firing in cerebellar nuclear neuron models, and expand a window current, causing severe childhood-onset cerebellar atrophy; both effects are blocked by the selective T-type blocker TTA-P2. Patch-clamp electrophysiology in transfected cells; computational cerebellar neuron modeling; whole-exome sequencing Brain High 29878067
2004 The gamma6 subunit (long and short isoforms) specifically inhibits CaV3.1 current density by ~49-69% in HEK-293 cells and reduces endogenous LVA current in HL-1 atrial cells by 63%, without affecting voltage dependence, kinetics, or CaV3.1 mRNA/protein levels; gamma4 and gamma7 have no effect on CaV3.1. Co-expression in HEK-293 cells; whole-cell patch-clamp; Western blot; RT-PCR; GFP-tagged subunit localization Journal of Molecular and Cellular Cardiology High 15572045
2008 The gamma6 subunit first transmembrane domain (TM1) contains a critical GxxxA motif required for physical association with CaV3.1 (confirmed by co-immunoprecipitation in HEK cells and atrial myocytes) and for reducing channel availability; mutational analysis of the GxxxA motif abolishes inhibitory function, indicating helix-helix interactions underlie gamma6 modulation of CaV3.1. Chimeric constructs; site-directed mutagenesis; co-immunoprecipitation; single-channel patch-clamp; whole-cell patch-clamp Journal of Physiology High 18818244
2009 An 8-amino acid peptide containing the GxxxA motif from gamma6 TM1 inhibits CaV3.1 current in a concentration-dependent, voltage-independent manner by dynamically binding/dissociating from the channel; both the GxxxA framework and surrounding aliphatic side-chains are required, consistent with interhelical interactions within the plasma membrane. Whole-cell electrophysiology; selective peptide mutagenesis Molecular Pharmacology High 19193827
2010 The LEF1/beta-catenin transcriptional complex binds four LEF1 sites in the proximal Cacna1g promoter in thalamic neurons in vivo (chromatin immunoprecipitation), activates promoter-driven luciferase reporter activity, and increases T-type current in thalamic neurons treated with WNT3A or LiCl. Chromatin immunoprecipitation (ChIP); luciferase reporter assay; DNase I footprinting; patch-clamp of cultured thalamic neurons; WNT pathway activation Journal of Neuroscience High 20371816
2008 Ni2+ blocks CaV3.1 pore by two mechanisms: a rapid, weakly voltage-dependent block (Kd ~1-3 mM, reduced by high permeant ion concentration) and a slow block (accelerated tail currents) that depends on permeant ion identity and concentration, with both components consistent with pore occlusion at distinct sites within the channel. Whole-cell patch-clamp; voltage-clamp; bimolecular kinetic analysis; ion substitution experiments Journal of General Physiology High 18663132
2008 Ca2+ and Ba2+ permeate CaV3.1 with similar apparent Kd values (~3 mM Ca2+, ~2.5 mM Ba2+); block by micromolar divalent cations is time-dependent; divalent cations shift channel activation via surface charge screening (1 e- per 98 Å2); Ba2+ accelerates inactivation by occupying the pore. Whole-cell patch-clamp; instantaneous I-V analysis; Gouy-Chapman-Stern surface charge modeling Journal of General Physiology High 18663131
2003 Extracellular protons shift CaV3.1 activation to more depolarized voltages and alter inactivation and deactivation kinetics; extracellular Ca2+ competes with protons for surface charges and for binding at the selectivity filter (EEDD pore locus mutation alters proton effects on selectivity); protons interact with intermediate closed states in the activation pathway. Whole-cell patch-clamp; pore-locus mutagenesis; model simulations; pH titration in HEK293 cells expressing CaV3.1 Journal of General Physiology High 12743167
2012 Fe2+ blocks CaV3.1 in a voltage-dependent manner (Kd 2.5 mM at 0 mV) competing with Ca2+ at the pore, and permeates the channel carrying measurable inward currents (~20 ions/s per open channel at -60 mV with 1 µM Fe2+), establishing CaV3.1 as a candidate pathway for non-transferrin-mediated Fe2+ influx. Whole-cell patch-clamp; instantaneous I-V; Woodhull and Eyring two-site/three-barrier modeling; HEK293 cells stably expressing CaV3.1 Molecular Pharmacology High 22973060
2012 Cd2+ blocks CaV3.1 in a voltage-dependent manner with relief at hyperpolarized potentials (suggesting pore permeation), carries sizable inward currents through the channel in the absence of other permeant ions, and radiolabeled 109Cd2+ uptake confirms cellular Cd2+ entry via CaV3.1. Whole-cell patch-clamp; instantaneous I-V; 109Cd2+ radiolabel uptake in HEK293 cells stably expressing CaV3.1 Molecular Pharmacology High 22973059
2006 Human CACNA1G undergoes extensive alternative splicing at 11 sites within the ORF plus 2 alternative promoters and 2 polyadenylation sites, generating 30 distinct transcripts; patch-clamp of 9 variants reveals combinatorial interactions between variable domains alter gating parameters; splicing patterns shift from biased/independent in fetal brain to strongly concerted in adult brain. Full-length cDNA transcript scanning (1580 cDNAs); statistical splice-site linkage analysis; whole-cell patch-clamp of selected variants; 5'-RACE Proteins High 16671074
2012 Beta-adrenergic stimulation (isoproterenol/cAMP analog) increases CaV3.1-mediated T-type Ca2+ current (ICa-T3.1) in cardiomyocytes via the cAMP/PKA pathway; this effect is blocked by H89 (PKA inhibitor) and is recapitulated in native SAN cells where CaV3.1 (not CaV3.2) mediates I(Ca-T). Patch-clamp of CaV3.1 transgenic cardiomyocytes and WT/KO SAN cells; pharmacological PKA inhibition; real-time PCR PLoS ONE High 22808078
2015 Cyclin-dependent kinase 5 (Cdk5) upregulates CaV3.1 T-type Ca2+ current; overexpression of Cdk5 increases macroscopic currents in HEK-293 cells stably expressing CaV3.1 and in N1E-115 neuroblastoma cells, while Cdk5 siRNA reduces them; site-directed mutagenesis identifies serine 2234 in the CaV3.1 C-terminal region as the major phosphorylation site. Whole-cell patch-clamp; Cdk5 overexpression/siRNA knockdown; site-directed mutagenesis (S2234); HEK-293 stable cells and N1E-115 cells PLoS ONE High 25760945
2010 CaV3.1 associates with the KV4.2-KChIP3-DPP10c complex and CaV3.1-mediated Ca2+ entry selectively right-shifts the inactivation voltage of KV4.2 into the physiological range; this regulation was not elicited by CaV1.4, CaV2.1, or CaV2.3, demonstrating T-type channel specificity. Heterologous co-expression; whole-cell patch-clamp; co-expression of channel complexes Channels Medium 20458163
2006 CaV3.1 controls thrombin-induced von Willebrand factor (VWF) secretion from pulmonary microvascular endothelial cells (PMVECs) but not pulmonary artery endothelial cells (PAECs); T-type blocker mibefradil and CaV3.1 shRNA knockdown nearly abolish thrombin-stimulated VWF-GFP vesicle exocytosis; recombinant CaV3.1 expression in PAECs confers mibefradil-sensitive Ca2+ entry and VWF secretion. GFP-tagged VWF real-time imaging; shRNA knockdown; mibefradil pharmacology; recombinant CaV3.1 overexpression; Ca2+ imaging American Journal of Physiology - Lung Cellular and Molecular Physiology High 17172292
2016 CaV3.1 mediates a substantial inward Ca2+ current at resting membrane potentials in T helper cells; CaV3.1 knockout mice are resistant to experimental autoimmune encephalomyelitis with reduced GM-CSF production by Th1/Th17 cells and decreased NFAT nuclear translocation, without affecting TCR-initiated Ca2+ entry. Patch-clamp of T cells; CaV3.1 KO mice; EAE model; NFAT localization; cytokine secretion assays Immunity High 27037192
2008 CaV3.1 knockout mice show attenuated neuropathic pain after L5 spinal nerve ligation, with reduced spontaneous pain responses, increased mechanical pain threshold, and reduced thermal hyperalgesia, establishing CaV3.1 as a required contributor to neuropathic pain development. CaV3.1 (alpha1G-/-) knockout mice; behavioral pain assays (spinal nerve ligation model); mechanical and thermal thresholds Molecules and Cells High 18414012
2016 Decreased Cacna1g expression partially ameliorates Scn1a+/- Dravet syndrome phenotype (improved survival, reduced spontaneous seizure frequency) while increased Cacna1g expression worsens Scn2aQ54 epilepsy (elevated seizure frequency), establishing Cacna1g as a genetic modifier that operates in epistasis with sodium channel genes. Transgenic alteration of Cacna1g expression in Scn1a+/- and Scn2aQ54 mouse models; seizure monitoring; survival analysis Epilepsia High 27112236 28556246
2010 CaV3.1 T-type Ca2+ channel is the dominant voltage-gated Ca2+ channel in mouse preadipocytes (C2C12 and primary); siRNA knockdown of alpha1G abolishes low-threshold Ca2+ current; mibefradil and NNC55-0396 block preadipocyte proliferation and prevent cell cycle entry/progression, while CaV3.1 expression decreases upon adipocyte differentiation. Patch-clamp; RT-PCR; Western blot; siRNA knockdown; immunohistochemistry; cell proliferation and cell cycle assays American Journal of Physiology - Cell Physiology High 20457833
2010 CaV3.1 T-type Ca2+ channel expression is upregulated in pulmonary artery smooth muscle cells by IGF-I through PI3K/Akt signaling; CaV3.1 knockdown (RNAi) prevents IGF-I-induced cyclin D expression/activation and cell cycle progression, linking T-type Ca2+ entry to mitogenic signaling. RT-PCR; Western blot; RNAi knockdown; patch-clamp; PI3K/Akt pathway inhibitors; cell cycle analysis American Journal of Physiology - Cell Physiology High 21148410
2006 Domain IV is the primary determinant of CaV3.1 vs. CaV3.3 differences in activation time constant and recovery from inactivation; domains I and IV together determine half-activation potential; the carboxy-terminal region is not involved; multiple domains collectively control inactivation kinetics. Chimeric channel constructs swapping transmembrane domains I-IV; whole-cell patch-clamp in tsA-201 cells Neuroscience High 16996222
2008 BMP4 upregulates CaV3.1 mRNA and T-type Ca2+ current in HL-1 atrial myocytes through a ROS/MAPK (JNK and p38) pathway involving NADPH oxidase-4 (NOX4); inhibitors of NADPH oxidase, radical scavengers, and JNK/p38 inhibitors block BMP4-induced CaV3.1 upregulation. Patch-clamp; real-time PCR; MAPK/NOX4 pathway inhibitors; noggin BMP4 inhibitor; HL-1 cells Pflugers Archiv Medium 24510064
2012 Overexpression of full-length CaV3.1 suppresses MCF-7 breast cancer cell proliferation and increases apoptosis (Annexin V/TUNEL positive cells localize CaV3.1 to plasma membrane); CaV3.1 knockdown promotes proliferation and blocks cyclophosphamide-induced apoptosis; CaV3.2 manipulation has no effect on proliferation. CaV3.1 overexpression and siRNA knockdown; apoptosis assays (Annexin V, TUNEL); immunocytochemistry; cell proliferation assays; ProTx-I pharmacology International Journal of Oncology Medium 22469755
2011 Roscovitine blocks CaV3.1 channels preferentially at depolarized voltages (EC50 10 µM) by negatively shifting closed-state inactivation voltage dependence, accelerating closed-state inactivation, and slowing recovery from inactivation, without major effects on open-state inactivation or deactivation. Transient expression in HEK293 cells; whole-cell patch-clamp; voltage protocols dissecting inactivation states Journal of Pharmacology and Experimental Therapeutics High 22088954
2008 CaV3.1 is expressed in the plasma membrane of outer hair cells (OHCs) in adult rat cochlea (but not inner hair cells at protein level); patch-clamp reveals a transient low-threshold inward Ca2+ current from -100 mV holding potential that is blocked by 1 µM mibefradil, establishing functional CaV3.1 T-type channel activity in mature OHCs. In situ hybridization; immunohistochemistry; Western blot; patch-clamp with mibefradil pharmacology Brain Research Medium 18294617
2021 CaV3.1 is predominantly localized in neuronal progenitor cells of the mouse hippocampal dentate gyrus; CaV3.1 knockout mice show decreased proliferation and survival of newly generated cells, impaired neuronal differentiation, reduced CaMKII and Akt phosphorylation, decreased BDNF expression, and impaired social interaction. CaV3.1 KO mice; BrdU cell labeling; doublecortin immunostaining; immunohistochemistry; Western blot; gene ontology analysis Acta Physiologica Medium 33393208
2022 CaV3.1 expression in dmVMH neurons mediates burst firing; optogenetically evoked burst firing induces anxiety-like behavior and shifts energy metabolism toward fat oxidation; Cav3.1 knockdown in dmVMH has opposite effects; fluoxetine blocks chronic stress-induced Cav3.1 upregulation and burst firing. Optogenetics; Cav3.1 knockdown; respiratory exchange ratio measurement; behavioral assays; in vivo electrophysiology Molecular Psychiatry High 35318460
2024 In human thalamocortical assembloids, the M1531V gain-of-function CACNA1G variant increases T-type currents in thalamic neurons and causes correlated hyperactivity of thalamic and cortical neurons; CACNA1G loss-of-function results in abnormal thalamocortical connectivity through increased spontaneous thalamic activity and aberrant axonal projections. Human iPSC-derived thalamocortical assembloids; patch-clamp; calcium imaging; axonal projection analysis; CACNA1G KO and GOF variant engineering Neuron High 39419023
2012 Insulin upregulates CaV3.1 T-type Ca2+ current in GH3 pituitary cells through increased endosomal recycling and membrane incorporation of channels, not via transcriptional upregulation; disruption of endosomal recycling by Brefeldin A or dominant-negative Rab11a prevents insulin's stimulatory effects. Patch-clamp; real-time RT-PCR; Western blot; luciferase reporter; Brefeldin A treatment; dominant-negative Rab11a expression in HEK-293/Cav3.1 cells Cell Calcium Medium 22770883
2022 CaV3.1 (but not CaV3.2) is required for stimulated ERK1/2 phosphorylation in response to serum, PDGF, and TGF-β1 in mouse mesangial cells; CRISPR-Cas9 knockout of CaV3.1 abolishes stimulated phospho-ERK1/2, whereas CaV3.2 KO retains these responses. CRISPR-Cas9 single/double KO of CaV3.1 and CaV3.2; ERK1/2 phosphorylation assays; proliferation assays; pharmacological TTCC inhibitors BMC Nephrology Medium 35710406
2018 CAV3.1 knockdown in prostate cancer cells inhibits proliferation, migration, and invasion by suppressing AKT activity, leading to decreased CCND1, N-cadherin, and Vimentin and increased E-cadherin; ectopic AKT expression rescues these effects. CAV3.1 siRNA knockdown; ectopic AKT expression rescue; CCK-8; cell cycle; transwell invasion; Western blot in prostate cancer cells Cancer Management and Research Medium 30410396
2003 The CACNA1G gene has two functional promoters (A and B) generating transcripts with different 5'-UTRs; promoter A is favored in undifferentiated Y79 cells and promoter B in differentiated cells; promoter A activity decreases during differentiation (with upstream enhancer/repressor sequences identified), explaining down-regulation of CaV3.1 expression during neuronal differentiation. RT-PCR; 5'-RACE; promoter-luciferase reporter assays; cloning of genomic DNA European Journal of Neuroscience Medium 12752779
2008 Dexamethasone (glucocorticoid) increases CaV3.1 mRNA and T-type Ca2+ current in neonatal cardiac myocytes through glucocorticoid receptor (GR) and NFκB; functional glucocorticoid response elements (GREs) are identified in the Cacna1g promoter, with GRE-1 mediating aldosterone response and GRE-4/GRE-5 mediating dexamethasone response. Patch-clamp; RT-PCR; promoter-luciferase reporter; site-directed mutagenesis of GREs; GR antagonist RU38486; NFκB inhibitor PDTC Molecular and Cellular Biochemistry Medium 18820838 19705257
2025 Leucine directly binds a hydrophobic pocket of the CaV3.1 voltage-sensing segment and lowers the threshold for voltage-dependent activation; pharmacological inhibition of CaV3.1 blunts leucine-induced POMC neuron activation; genetic deletion of Cacna1g in POMC neurons abolishes appetite- and weight-suppressive effects of high-protein feeding. Pharmacological inhibition in cultured neurons and brain slices; conditional Cacna1g KO in POMC neurons; in vivo hypothalamic leucine injection; diet-induced obesity model; structural binding analysis Cell Metabolism High 42025169
2025 CACNA1G loss-of-function in Xenopus tropicalis reduces cilia quantity in the left-right organizer (LRO), causing disrupted LR patterning markers (pitx2c and dand5) and cardiac looping defects, establishing a role for CaV3.1 in ciliogenesis and LR asymmetry. CRISPR crispants in Xenopus tropicalis; in situ hybridization of LR markers; morphological analysis of LRO cilia; cardiac looping assessment Genesis Medium 40008628
2011 CaV3.1 knockout in the alpha1 GABAA receptor null background (double mutant mice) causes severe motor abnormalities, potentiated tremor at 20 Hz refractory to propranolol, and age-dependent loss of cerebellar Purkinje neurons, revealing a role for CaV3.1 in motor coordination under pathological conditions. Double knockout mice (alpha1-/- / alpha1G-/-); tremor activity measurement; rotarod motor learning; propranolol pharmacology; cerebellar histology Biochemical and Biophysical Research Communications Medium 21621520

Source papers

Stage 0 corpus · 89 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2006 Bradycardia and slowing of the atrioventricular conduction in mice lacking CaV3.1/alpha1G T-type calcium channels. Circulation research 231 16690884
2005 Thalamic Cav3.1 T-type Ca2+ channel plays a crucial role in stabilizing sleep. Proceedings of the National Academy of Sciences of the United States of America 158 15677322
1999 Inactivation of CACNA1G, a T-type calcium channel gene, by aberrant methylation of its 5' CpG island in human tumors. Cancer research 132 10493502
2009 Functional coupling between mGluR1 and Cav3.1 T-type calcium channels contributes to parallel fiber-induced fast calcium signaling within Purkinje cell dendritic spines. The Journal of neuroscience : the official journal of the Society for Neuroscience 86 19657020
2015 A Recurrent Mutation in CACNA1G Alters Cav3.1 T-Type Calcium-Channel Conduction and Causes Autosomal-Dominant Cerebellar Ataxia. American journal of human genetics 85 26456284
2015 A mutation in the low voltage-gated calcium channel CACNA1G alters the physiological properties of the channel, causing spinocerebellar ataxia. Molecular brain 82 26715324
2018 De novo mutation screening in childhood-onset cerebellar atrophy identifies gain-of-function mutations in the CACNA1G calcium channel gene. Brain : a journal of neurology 79 29878067
2003 Immunological characterization of T-type voltage-dependent calcium channel CaV3.1 (alpha 1G) and CaV3.3 (alpha 1I) isoforms reveal differences in their localization, expression, and neural development. Neuroscience 72 12614673
2012 T-type voltage-activated calcium channel Cav3.1, but not Cav3.2, is involved in the inhibition of proliferation and apoptosis in MCF-7 human breast cancer cells. International journal of oncology 68 22469755
2007 Mutational analysis of CACNA1G in idiopathic generalized epilepsy. Mutation in brief #962. Online. Human mutation 65 17397049
2010 LEF1/beta-catenin complex regulates transcription of the Cav3.1 calcium channel gene (Cacna1g) in thalamic neurons of the adult brain. The Journal of neuroscience : the official journal of the Society for Neuroscience 55 20371816
2006 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 53 16671074
2009 High-density SNP association study of the 17q21 chromosomal region linked to autism identifies CACNA1G as a novel candidate gene. Molecular psychiatry 51 19455149
2013 Age-related downregulation of the CaV3.1 T-type calcium channel as a mediator of amyloid beta production. Neurobiology of aging 46 24268883
2017 Cacna1g is a genetic modifier of epilepsy in a mouse model of Dravet syndrome. Epilepsia 45 28556246
2008 Attenuated neuropathic pain in Cav3.1 null mice. Molecules and cells 40 18414012
2023 LncRNA CACNA1G-AS1 up-regulates FTH1 to inhibit ferroptosis and promote malignant phenotypes in ovarian cancer cells. Oncology research 39 37304234
2016 Ontogenic Changes and Differential Localization of T-type Ca(2+) Channel Subunits Cav3.1 and Cav3.2 in Mouse Hippocampus and Cerebellum. Frontiers in neuroanatomy 39 27616982
2016 Cacna1g is a genetic modifier of epilepsy caused by mutation of voltage-gated sodium channel Scn2a. Epilepsia 38 27112236
2010 Regulation of the KV4.2 complex by CaV3.1 calcium channels. Channels (Austin, Tex.) 36 20458163
2017 Transcriptome analysis of PDGFRα+ cells identifies T-type Ca2+ channel CACNA1G as a new pathological marker for PDGFRα+ cell hyperplasia. PloS one 34 28806761
2016 Low-Voltage-Activated CaV3.1 Calcium Channels Shape T Helper Cell Cytokine Profiles. Immunity 34 27037192
2022 Cav3.1-driven bursting firing in ventromedial hypothalamic neurons exerts dual control of anxiety-like behavior and energy expenditure. Molecular psychiatry 32 35318460
2005 Subtype switching of T-type Ca 2+ channels from Cav3.2 to Cav3.1 during differentiation of embryonic stem cells to cardiac cell lineage. Circulation journal : official journal of the Japanese Circulation Society 32 16195632
2004 Calcium channel gamma6 subunits are unique modulators of low voltage-activated (Cav3.1) calcium current. Journal of molecular and cellular cardiology 32 15572045
2012 Fe²⁺ block and permeation of CaV3.1 (α1G) T-type calcium channels: candidate mechanism for non-transferrin-mediated Fe²⁺ influx. Molecular pharmacology 31 22973060
2024 Human assembloids reveal the consequences of CACNA1G gene variants in the thalamocortical pathway. Neuron 30 39419023
2008 Ni2+ block of CaV3.1 (alpha1G) T-type calcium channels. The Journal of general physiology 28 18663132
2018 Long non-coding RNA CACNA1G-AS1 promotes cell migration, invasion and epithelial-mesenchymal transition by HNRNPA2B1 in non-small cell lung cancer. European review for medical and pharmacological sciences 27 29509247
2013 Bisphenol A differently inhibits CaV3.1, Ca V3.2 and Ca V3.3 calcium channels. Naunyn-Schmiedeberg's archives of pharmacology 27 24170242
2003 Extracellular Ca2+ modulates the effects of protons on gating and conduction properties of the T-type Ca2+ channel alpha1G (CaV3.1). The Journal of general physiology 26 12743167
2012 Cd²⁺ block and permeation of CaV3.1 (α1G) T-type calcium channels: candidate mechanism for Cd²⁺ influx. Molecular pharmacology 25 22973059
2012 β-Adrenergic stimulation increases Cav3.1 activity in cardiac myocytes through protein kinase A. PloS one 24 22808078
2010 Regulation and function of Cav3.1 T-type calcium channels in IGF-I-stimulated pulmonary artery smooth muscle cells. American journal of physiology. Cell physiology 24 21148410
2006 Cav3.1 (alpha1G) controls von Willebrand factor secretion in rat pulmonary microvascular endothelial cells. American journal of physiology. Lung cellular and molecular physiology 24 17172292
2010 Involvement of CaV3.1 T-type calcium channels in cell proliferation in mouse preadipocytes. American journal of physiology. Cell physiology 23 20457833
2006 Determinants of the differential gating properties of Cav3.1 and Cav3.3 T-type channels: a role of domain IV? Neuroscience 22 16996222
2003 Regulation of alpha1G T-type calcium channel gene (CACNA1G) expression during neuronal differentiation. The European journal of neuroscience 22 12752779
2020 Channelopathies of voltage-gated L-type Cav1.3/α1D and T-type Cav3.1/α1G Ca2+ channels in dysfunction of heart automaticity. Pflugers Archiv : European journal of physiology 21 32601767
2019 Infantile-Onset Syndromic Cerebellar Ataxia and CACNA1G Mutations. Pediatric neurology 21 31836334
2008 Permeation and gating in CaV3.1 (alpha1G) T-type calcium channels effects of Ca2+, Ba2+, Mg2+, and Na+. The Journal of general physiology 21 18663131
2015 Regulation of neuronal cav3.1 channels by cyclin-dependent kinase 5 (Cdk5). PloS one 19 25760945
2020 Long non-coding RNA CACNA1G-AS1 promotes proliferation and invasion and inhibits apoptosis by regulating expression of miR-205 in human keloid fibroblasts. Bioscience reports 18 32495824
2019 LncRNA CACNA1G-AS1 facilitates hepatocellular carcinoma progression through the miR-2392/C1orf61 pathway. Journal of cellular physiology 18 30908634
2018 A case of a novel CACNA1G mutation from a Chinese family with SCA42: A case report and literature review. Medicine 18 30200108
2020 Novel Missense CACNA1G Mutations Associated with Infantile-Onset Developmental and Epileptic Encephalopathy. International journal of molecular sciences 17 32878331
2008 A critical GxxxA motif in the gamma6 calcium channel subunit mediates its inhibitory effect on Cav3.1 calcium current. The Journal of physiology 17 18818244
2008 Regulation of T-type Cav3.1 channels expression by synthetic glucocorticoid dexamethasone in neonatal cardiac myocytes. Molecular and cellular biochemistry 17 18820838
2015 CaV3.1 T-Type Ca2+ Channels Contribute to Myogenic Signaling in Rat Retinal Arterioles. Investigative ophthalmology & visual science 16 26241400
2018 CAV3.1 knockdown suppresses cell proliferation, migration and invasion of prostate cancer cells by inhibiting AKT. Cancer management and research 15 30410396
2010 Different distribution of Cav3.2 and Cav3.1 transcripts encoding T-type Ca(2+) channels in the embryonic heart of mice. Biomedical research (Tokyo, Japan) 15 21079360
2005 T-type calcium channel trigger p21ras signaling pathway to ERK in Cav3.1-expressed HEK293 cells. Brain research 15 16054119
2005 Inorganic mercury and methylmercury inhibit the Cav3.1 channel expressed in human embryonic kidney 293 cells by different mechanisms. The Journal of pharmacology and experimental therapeutics 15 16326920
2009 Expanded alternative splice isoform profiling of the mouse Cav3.1/alpha1G T-type calcium channel. BMC molecular biology 14 19480703
2006 Transforming growth factor-beta1 and bone morphogenetic protein-2 downregulate CaV3.1 channel expression in mouse C2C12 myoblasts. Journal of cellular physiology 14 16883604
2020 De novo CACNA1G variants in developmental delay and early-onset epileptic encephalopathies. Journal of the neurological sciences 13 32736238
2021 Overexpression of T-type calcium channel Cav3.1 in oral squamous cell carcinoma: association with proliferation and anti-apoptotic activity. Journal of molecular histology 12 33394292
2011 Lack of CaV3.1 channels causes severe motor coordination defects and an age-dependent cerebellar atrophy in a genetic model of essential tremor. Biochemical and biophysical research communications 12 21621520
2020 Upregulated lncRNA CACNA1G-AS1 aggravates the progression of colorectal cancer by downregulating p53. European review for medical and pharmacological sciences 11 31957825
2008 The CaV3.1 T-type Ca2+channel contributes to voltage-dependent calcium currents in rat outer hair cells. Brain research 11 18294617
2011 Roscovitine inhibits CaV3.1 (T-type) channels by preferentially affecting closed-state inactivation. The Journal of pharmacology and experimental therapeutics 10 22088954
2021 Cav3.1 t-type calcium channel is critical for cell proliferation and survival in newly generated cells of the adult hippocampus. Acta physiologica (Oxford, England) 9 33393208
2018 Up-regulation of Cav3.1 expression in SH-SY5Y cells induced by lidocaine hydrochloride. Artificial cells, nanomedicine, and biotechnology 9 29327607
2006 Gating of the expressed T-type Cav3.1 calcium channels is modulated by Ca2+. Acta physiologica (Oxford, England) 9 16634780
2014 Bone morphogenetic protein-4 induces upregulation of Cav3.1 Ca²⁺ channels in HL-1 atrial myocytes. Pflugers Archiv : European journal of physiology 8 24510064
2022 Computational epigenetic landscape analysis reveals association of CACNA1G-AS1, F11-AS1, NNT-AS1, and MSC-AS1 lncRNAs in prostate cancer progression through aberrant methylation. Scientific reports 7 35715447
2015 Compensatory reduction of Cav3.1 expression in thalamocortical neurons of juvenile rats of WAG/Rij model of absence epilepsy. Epilepsy research 6 26656778
2012 Insulin-mediated upregulation of T-type Ca2+ currents in GH3 cells is mediated by increased endosomal recycling and incorporation of surface membrane Cav3.1 channels. Cell calcium 6 22770883
2009 A small peptide inhibitor of the low voltage-activated calcium channel Cav3.1. Molecular pharmacology 6 19193827
2021 The T-type Calcium Channel Cav3.1 in Y79 Retinoblastoma Cells is Regulated by the Epidermal Growth Factor Receptor via the MAPK Signaling Pathway. Current eye research 5 34674590
2008 The relationship between single-channel and whole-cell conductance in the T-type Ca2+ channel CaV3.1. Biophysical journal 5 18375519
2024 The characterization of new de novo CACNA1G variants affecting the intracellular gate of Cav3.1 channel broadens the spectrum of neurodevelopmental phenotypes in SCA42ND. Genetics in medicine : official journal of the American College of Medical Genetics 4 39674904
2021 Downregulation of Cav3.1 T-type Calcium Channel Expression in Age-related Hearing Loss Model. Current medical science 4 34403092
2023 CD19, ALDH18A1, and CACNA1G as Significant Hub Genes in End-Stage Osteoarthritis. Iranian journal of public health 3 38435769
2009 Identification of functional corticosteroid response elements involved in regulation of Cacna1g expression in cardiac myocytes. Molecular and cellular biochemistry 3 19705257
2022 Knockdown of the long non-coding RNA CACNA1G-AS1 enhances cytotoxicity and apoptosis of human diffuse large B cell lymphoma by regulating miR-3160-5p. Experimental and therapeutic medicine 2 36160896
2022 Paroxysmal Tonic Upgaze in a Patient With Congenital Ataxia due to a De Novo Missense Variant of CACNA1G. Pediatric neurology 2 36508879
2018 Short- and long-term roles of phosphatidylinositol 4,5-bisphosphate PIP2 on Cav3.1- and Cav3.2-T-type calcium channel current. Pathophysiology : the official journal of the International Society for Pathophysiology 2 30528337
2013 Construction and identification of the pshRNA-CACNA1G-SH-SY5Ycells targeted to silence Cav3.1 mRNA expression. Biomedical reports 2 24649007
2025 CACNA1G, A Heterotaxy Candidate Gene, Plays a Role in Ciliogenesis and Left-Right Patterning in Xenopus tropicalis. Genesis (New York, N.Y. : 2000) 1 40008628
2025 The Functional Interplay among GAD2, GABRG2, and CACNA1G Genes in Cancers. Asian Pacific journal of cancer prevention : APJCP 1 40849687
2024 CACNA1G Causes Dominantly Inherited Myoclonus-Ataxia with Intellectual Disability: A Case Report. Cerebellum (London, England) 1 39287920
2022 Stimulated phosphorylation of ERK in mouse kidney mesangial cells is dependent upon expression of Cav3.1. BMC nephrology 1 35710406
2021 Variant in CACNA1G as a Possible Genetic Modifier of Neonatal Epilepsy in an Infant with a De Novo SCN2A Mutation. Journal of pediatric genetics 1 37090830
2020 Expression and functions of N-type Cav2.2 and T-type Cav3.1 channels in rat vasopressin neurons under normotonic conditions. The journal of physiological sciences : JPS 1 33059597
2026 Cav3.1 is a neuronal leucine sensor that mediates satiety and weight loss in response to dietary protein. Cell metabolism 0 42025169
2025 Electrophysiological classification of CACNA1G gene variants associated with neurodevelopmental and neurological disorders. Frontiers in pharmacology 0 41111510
2024 Unmasking early colorectal cancer clues: in silico and in vitro investigation of downregulated IGF2, SOCS1, MLH1, and CACNA1G in SSA polyps. Molecular biology reports 0 38874740
2020 The expression of Cav3.1 on T-type calcium channels of rats with subarachnoid hemorrhage. Saudi journal of biological sciences 0 32565706