Affinage

CACNA1H

Voltage-dependent T-type calcium channel subunit alpha-1H · UniProt O95180

Length
2353 aa
Mass
259.2 kDa
Annotated
2026-06-09
100 papers in source corpus 50 papers cited in narrative 50 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CACNA1H encodes Cav3.2, a low-voltage-activated T-type calcium channel that converts membrane depolarization near resting potential into Ca2+ influx, supporting burst firing, nociceptive signaling, and Ca2+-driven gene programs across neurons, adrenal cortex, cartilage, heart, and vasculature (PMID:15616581, PMID:19052226, PMID:24778262). Its biophysical gating is tuned by a dense regulatory layer: in vivo phosphorylation at 34 sites (including a I-II loop cluster S442/S445/T446) shapes activation and inactivation (PMID:26483470), PKA augments current via the II-III loop and licenses voltage-independent Gβγ inhibition through Ser1107 (PMID:16569752, PMID:19131331), and an extracellular metal-binding site organized around His191 in IS3-S4 mediates selective redox modulation by zinc, nitrous oxide, H2S, and CO that distinguishes Cav3.2 from Cav3.1/Cav3.3 (PMID:19940152, PMID:21059758, PMID:25183670, PMID:23671274). Channel surface density is set by competing trafficking and stability machinery: N-glycosylation at N192 governs surface expression and N1466 governs activity (PMID:23503728), calnexin binding at the III-IV linker controls ER sorting (PMID:28912545), and the same linker is ubiquitinated by WWP1 and deubiquitinated/stabilized by USP5, a balance that controls plasma-membrane levels and pain signaling (PMID:25189210). In nociceptive Aδ/C-fiber DRG and trigeminal neurons, Cav3.2 is the dominant T-type isoform and its upregulation drives inflammatory and neuropathic pain, with knockdown producing analgesia (PMID:15616581, PMID:25600872, PMID:23867767); multiple GPCRs and inflammatory mediators converge on the channel to modulate this output (PMID:18292205, PMID:19805509, PMID:29437250, PMID:34646374). Gain-of-function gating changes are pathogenic in two settings: mutations that hyperpolarize activation or slow inactivation (e.g., F161L, E282K, M1549V, C456S) increase neuronal Ca2+ influx and NMDA receptor-mediated transmission to cause absence epilepsy (PMID:14729682, PMID:15888660, PMID:26220996), while gain-of-function mutations such as M1549V raise glomerulosa intracellular Ca2+ to drive CYP11B2-dependent aldosterone production, causing primary aldosteronism (PMID:25907736, PMID:27729216, PMID:33879608). Beyond these, Cav3.2-derived Ca2+ activates calcineurin/NFAT/Sox9 signaling required for tracheal chondrogenesis (PMID:24778262) and feeds a CaV3.2→ryanodine receptor→BKCa negative-feedback axis restraining arterial myogenic tone (PMID:26069238).

Mechanistic history

Synthesis pass · year-by-year structured walk · 16 steps
  1. 2004 High

    Established that Cav3.2 itself, not merely a generic T-type current, drives nociception, providing the founding gene-function link for the pain field.

    Evidence Intrathecal antisense knockdown in rat DRG with electrophysiology and behavioral pain assays

    PMID:15616581

    Open questions at the time
    • Does not resolve subcellular site of action
    • Antisense specificity vs other Cav3 isoforms not fully excluded
  2. 2004 High

    Defined how human absence-epilepsy mutations alter channel biophysics, linking specific gating shifts to pathogenic Ca2+ influx near rest.

    Evidence Site-directed mutagenesis (F161L, E282K, V831M) and whole-cell patch clamp in HEK293

    PMID:14729682

    Open questions at the time
    • In vitro only; no in vivo seizure correlation
    • Splice-variant context not tested
  3. 2005 High

    Systematically scaled the genotype-to-gating analysis, showing most CAE variants alter gating and predicting their net effect on firing, establishing them as functional susceptibility alleles.

    Evidence Mutagenesis of 12 variants, patch clamp, and computational neuronal modeling

    PMID:15888660

    Open questions at the time
    • Firing predictions are computational
    • No animal validation in this study
  4. 2006 High

    Identified Cav3.2 as the selective molecular substrate for redox modulation of T-type current and mapped PKA augmentation to the II-III loop, opening the channel's regulatory-domain architecture.

    Evidence Native thalamic neuron and recombinant recordings with Cav3.2-null mice; chimeric Nav1.4/Cav3.2 channels in oocytes

    PMID:16569752 PMID:16644797

    Open questions at the time
    • Redox sensor residue not yet identified in 2006
    • PKA target residue not yet mapped
  5. 2009 High

    Resolved the molecular logic of GPCR and Gβγ regulation, showing PKA phosphorylation of Ser1107 is a prerequisite for voltage-independent Gβγ inhibition, and identified the His191 metal-binding pocket controlling gating.

    Evidence S1107A mutagenesis with single-channel recording; chimera/mutagenesis zinc-block assays

    PMID:18292205 PMID:19131331 PMID:19805509 PMID:19940152

    Open questions at the time
    • Stoichiometry of Gβγ binding vs phosphorylation not quantified
    • Physiological GPCR coupling in native nociceptors inferred from heterologous systems
  6. 2008 High

    Demonstrated that transcriptional upregulation of Cav3.2 is a causal step in epileptogenesis, moving the channel from biophysical correlate to driver of network pathology.

    Evidence Cav3.2-null mice with qPCR, patch clamp, EEG, and histopathology after status epilepticus

    PMID:19052226

    Open questions at the time
    • Upstream transcriptional trigger not identified in this study
    • Cell types responsible not dissected
  7. 2010 High

    Mechanistically explained gasotransmitter and anesthetic modulation by showing His191 forms a metal/ROS-sensitive site, unifying N2O, H2S, CO, and S-nitrosothiol regulation of Cav3.2.

    Evidence H191 and cysteine mutagenesis, ROS scavengers, Zn2+ chelation, native DRG recordings, Cav3.2-null behavior

    PMID:21059758 PMID:23671274 PMID:23813099 PMID:25183670

    Open questions at the time
    • Endogenous redox tone regulating the site in vivo not fully quantified
    • Whether thioredoxin acts directly on H191 unresolved
  8. 2012 High

    Identified the transcriptional control of Cacna1h by an Egr1 (activator)/REST (repressor) module, providing the gene-regulatory layer governing channel abundance.

    Evidence Promoter reporter assays, ChIP in cells and mouse hippocampus, electrophysiology

    PMID:22431737

    Open questions at the time
    • Tissue-specific deployment of this module not mapped
    • Signals upstream of Egr1/REST not defined here
  9. 2013 High

    Extended the regulatory network to cardiac hypertrophy and Ca2+/calmodulin signaling, showing Egr1-driven Cav3.2 upregulation under pressure overload and a reciprocal Cav3.2-calcineurin physical interaction.

    Evidence ChIP/EMSA, in vivo cardiac gene transfer, siRNA/rescue; Co-IP and calcineurin phosphatase activity assays with peptide inhibition

    PMID:23669360 PMID:23929524

    Open questions at the time
    • Calcineurin-binding site on Cav3.2 not residue-mapped
    • Causality of Cav3.2 in adult cardiac disease in vivo not fully established
  10. 2014 High

    Showed Cav3.2-derived Ca2+ drives a developmental transcriptional program (calcineurin/NFAT/Sox9) required for chondrogenesis, broadening the channel's role beyond excitable signaling.

    Evidence Cav3.2-null mice, ATDC5 overexpression, NFAT inhibitors, luciferase/EMSA/ChIP on Sox9 promoter

    PMID:24778262

    Open questions at the time
    • How Ca2+ influx is gated in non-excitable chondrocytes unclear
    • Other NFAT target genes not surveyed
  11. 2014 High

    Defined the trafficking/stability machinery controlling surface Cav3.2, identifying WWP1 ubiquitination and USP5 deubiquitination at the III-IV linker as the determinant of pain-relevant channel density.

    Evidence Proteomic screen, reciprocal Co-IP, shRNA, Tat peptide uncoupling, patch clamp and behavior

    PMID:25189210

    Open questions at the time
    • Specific ubiquitinated lysines only partially defined
    • Regulation of WWP1/USP5 activity in disease states addressed later
  12. 2015 High

    Provided the in vivo phosphorylation map and post-translational/trafficking controls (glycosylation, calnexin), defining how channel gating and surface delivery are set biochemically.

    Evidence Brain immunopurification phosphoproteomics with mutagenesis; N-glycosylation mutagenesis with biotinylation; calnexin Co-IP and surface assays

    PMID:23503728 PMID:26483470 PMID:28912545

    Open questions at the time
    • Kinases responsible for individual sites largely unassigned
    • Quantitative contribution of each site to native current unknown
  13. 2015 High

    Connected gain-of-function gating directly to disease physiology: M1549V drives autonomous aldosterone production, and CAE-linked C456S enhances synaptic NMDA transmission and induces spike-wave discharges in vivo.

    Evidence Exome sequencing and patch clamp of mutants; synaptic recordings, in vivo cortical expression, EEG; cell-type-specific Cav3.2 conditional knockout

    PMID:25600872 PMID:25907736 PMID:26220996

    Open questions at the time
    • How channel localizes to synapses/active zones mechanistically incomplete
    • Translation of rodent epilepsy phenotype to human variant penetrance not addressed
  14. 2016 High

    Generalized the aldosteronism mechanism across multiple CACNA1H variants and demonstrated pharmacological reversibility, linking channel gain-of-function to CYP11B2 induction.

    Evidence Patch clamp of four variants plus M1549V in adrenocortical cells, aldosterone ELISA, CYP11B2 PCR, mibefradil rescue

    PMID:27258646 PMID:27729216

    Open questions at the time
    • Cellular Ca2+ signaling chain not yet directly imaged here
    • Adrenal in vivo confirmation came later
  15. 2021 High

    Closed the mechanistic chain in primary aldosteronism in vivo, showing knockin M1549V raises glomerulosa intracellular Ca2+, aldosterone, and blood pressure.

    Evidence CRISPR knockin/knockout mice, BP telemetry, aldosterone/renin assays, adrenal slice Ca2+ imaging

    PMID:33879608

    Open questions at the time
    • Downstream Ca2+ effector pathway to CYP11B2 in vivo not fully dissected
    • Modest BP effect leaves room for compensatory mechanisms
  16. 2022 Medium

    Identified epigenetic/miRNA control of Cav3.2 in neuropathic pain, showing chromatin-silencing of miR-32-5p de-represses Cav3.2 to drive trigeminal pain.

    Evidence miRNA sequencing, histone methyltransferase inhibitors, lentiviral miRNA overexpression, patch clamp, behavior; plus USP5-SUMO and IL-1β/USP5 pain studies

    PMID:28741432 PMID:31455361 PMID:35353623

    Open questions at the time
    • Single-lab findings without independent replication
    • Relative contribution of transcriptional vs trafficking control to pain-state upregulation unresolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the many overlapping regulatory inputs (phosphorylation, glycosylation, ubiquitination/SUMO, redox, GPCR signaling, transcriptional and miRNA control) are integrated to set Cav3.2 function in a given cell type, and the structural basis of these modulations, remains unresolved.
  • No high-resolution structure of regulated states in the corpus
  • Quantitative hierarchy among regulators in native tissue undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140299 molecular sensor activity 5 GO:0005215 transporter activity 4
Localization
GO:0005886 plasma membrane 3 GO:0005783 endoplasmic reticulum 1
Pathway
R-HSA-1430728 Metabolism 4 R-HSA-112316 Neuronal System 3
Partners
CALRHCN1KCNMA1PPP3CAUSP5WWP1

Evidence

Reading pass · 50 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2004 Intrathecal antisense knockdown of Cav3.2 mRNA and protein in dorsal root ganglion neurons reduces 'Cav3.2-like' T-type currents and produces antinociceptive, anti-hyperalgesic, and anti-allodynic effects in rats, directly linking Cav3.2 to pain perception. Antisense oligodeoxynucleotide knockdown in vivo, electrophysiology, behavioral nociceptive assays The EMBO journal High 15616581
2014 Cav3.2 T-type channels are ubiquitinated by the plasma-membrane-associated E3 ubiquitin ligase WWP1, which binds the intracellular domain III-IV linker region of Cav3.2 and modifies specific lysine residues there; the deubiquitinating enzyme USP5 also binds the III-IV linker (identified by proteomic screen), counteracts WWP1-mediated ubiquitination, stabilizes Cav3.2 protein levels, and maintains Cav3.2 whole-cell currents and nociceptive signaling. Proteomic screen, Co-IP, shRNA knockdown, whole-cell patch clamp, in vivo Tat peptide delivery with behavioral assays Neuron High 25189210
2015 The gain-of-function CACNA1H M1549V mutation drastically impairs Cav3.2 channel inactivation and shifts activation to more hyperpolarized potentials, increasing intracellular Ca2+ and driving autonomous aldosterone production, causing early-onset hypertension with primary aldosteronism. Exome sequencing, whole-cell patch clamp of mutant channels expressed in HEK cells, electrophysiological characterization eLife High 25907736
2008 Transient selective upregulation of Cav3.2 mRNA and protein after status epilepticus increases T-type Ca2+ currents and burst firing; Cav3.2-null mice lack these changes and show dramatically reduced spontaneous seizures, neuron loss, and mossy fiber sprouting, establishing Cav3.2 transcriptional upregulation as a critical step in epileptogenesis. Cav3.2 knockout mice, qPCR, western blot, whole-cell patch clamp, in vivo EEG seizure monitoring, histopathology The Journal of neuroscience High 19052226
2006 Cav3.2 channels are the primary molecular substrate for redox regulation of T-type Ca2+ currents in thalamic neurons: reducing agents selectively enhance Cav3.2 (but not Cav3.1 or Cav3.3) currents, and this enhancement is absent in Cav3.2-null mice. Patch clamp electrophysiology in native thalamic neurons and recombinant channels, Cav3.2 knockout mice The Journal of physiology High 16644797
2004 Childhood absence epilepsy-associated missense mutations F161L and E282K in Cav3.2 shift the half-activation potential ~10 mV hyperpolarized (allowing channel opening near resting potential); V831M slows inactivation ~50% and shifts half-inactivation ~10 mV depolarized—all increasing calcium influx during physiological activation. Site-directed mutagenesis of rat Cav3.2, whole-cell patch clamp in transfected HEK293 cells The Journal of biological chemistry High 14729682
2005 Eleven of twelve CAE-associated Cav3.2 SNPs alter channel gating properties when introduced into recombinant channels; computer modeling predicts that seven increase neuronal firing (three inducing oscillations at absence-seizure frequencies) and three decrease firing, establishing these as susceptibility variants that alter channel function. Site-directed mutagenesis, whole-cell patch clamp in transfected cells, computational neuronal modeling The Journal of neuroscience High 15888660
2015 N-linked glycosylation at asparagine N192 of Cav3.2 is critical for surface expression of the channel, whereas glycosylation at N1466 controls channel activity; N-glycosylation also underlies glucose-dependent potentiation of T-type current. Site-directed mutagenesis of N-glycosylation sites, surface biotinylation, whole-cell patch clamp in recombinant expression system Pflugers Archiv High 23503728
2009 The high-affinity extracellular zinc/metal binding site on Cav3.2 is formed by a His-Gly-Asp motif in IS3-S4 (with H191 as critical histidine) together with an aspartate in IS2; this site stabilizes the closed conformation of the voltage-sensor paddle in repeat I to inhibit channel opening. Chimeric channel construction, site-directed mutagenesis, whole-cell patch clamp electrophysiology with zinc/metal block assays The Journal of biological chemistry High 19940152
2015 In vivo phosphorylation mapping of Cav3.2 immunopurified from rat brain identified 34 phosphorylation sites; phosphorylation directly regulates channel gating including voltage-dependent activation, inactivation, and kinetics. A cluster at S442/S445/T446 in the loop I-II is crucial for this regulation, shown by alkaline phosphatase treatment and dephosphomimetic mutants. Immunopurification from rat brain, high-resolution mass spectrometry phosphoproteomics, site-directed mutagenesis, patch clamp electrophysiology Proceedings of the National Academy of Sciences of the United States of America High 26483470
2006 PKA augments Cav3.2 channel activity (~40%) and negatively shifts steady-state inactivation; the PKA-mediated augmentation is localized to the II-III intracellular loop of Cav3.2, identified using chimeric channels with Nav1.4 segments. Xenopus oocyte expression, whole-cell patch clamp, pharmacological PKA activation/inhibition, chimeric channel construction The Journal of pharmacology and experimental therapeutics High 16569752
2009 Gβγ dimers inhibit Cav3.2 channels in a voltage-independent manner that requires prior PKA phosphorylation of Ser1107 on the II-III loop; S1107A mutation prevents Gβγ inhibition without disrupting dimer binding. Dopamine inhibits Cav3.2 via synergistic D1/D2 receptor activation requiring both PKA and Gβγ. Site-directed mutagenesis (S1107A), single-channel and whole-cell patch clamp, recombinant Gβγ application, pharmacological dopamine receptor manipulation The Journal of biological chemistry High 19131331
2008 CRFR1 activation by CRF or urocortin 1 selectively inhibits Cav3.2 (but not Cav3.1 or Cav3.3) currents via a cholera toxin-sensitive Gβγ-dependent mechanism; inhibition is independent of PLC, tyrosine kinases, CaMKII, or PKC, and manifests as a hyperpolarizing shift in steady-state inactivation. Whole-cell patch clamp, pharmacological dissection with pathway inhibitors, selective receptor antagonist (astressin), co-expression of CRFR1 with Cav3 isoforms Molecular pharmacology High 18292205
2009 NK1 receptor inhibits Cav3.2 channels through a voltage-independent Gαq/11-PLC-PKC signaling pathway; dominant-negative Gαq, RGS2/3T, U73122 (PLC inhibitor), and bisindolylmaleimide I (PKC inhibitor) each block the inhibition, whereas Gαt (Gβγ scavenger) does not. Co-expression in HEK293 cells, whole-cell patch clamp, dominant-negative constructs, pharmacological inhibitors of PLC and PKC Molecular pharmacology High 19805509
2014 Cav3.2 is required for tracheal chondrogenesis: Cav3.2-null mice have congenital tracheal stenosis due to incomplete cartilage formation. Ca2+ influx via Cav3.2 activates calcineurin/NFAT signaling, and NFAT binds a newly identified site in the Sox9 promoter to drive Sox9 expression during chondrogenesis. Cav3.2 knockout mice, Cav3.2 overexpression in ATDC5 cells, calcineurin/NFAT inhibitors, luciferase reporter assay, gel shift (EMSA), ChIP Proceedings of the National Academy of Sciences of the United States of America High 24778262
2012 The transcription factor Egr1 activates the Cav3.2 (Cacna1h) promoter by binding to multiple Egr1 sites identified therein; REST (NRSF) counteracts Egr1 and represses Cav3.2 promoter activity and mRNA. Egr1 overexpression in vitro and in vivo increases Cav3.2 mRNA and T-type current. Promoter analysis, dual-luciferase reporter assay, chromatin immunoprecipitation (ChIP) in NG108-15 cells and mouse hippocampi, whole-cell patch clamp The Journal of biological chemistry High 22431737
2016 Electrophysiological analysis of four novel CACNA1H variants associated with different forms of primary aldosteronism (p.Met1549Ile, p.Ser196Leu, p.Pro2083Leu, p.Val1951Glu) all show significant gain-of-function changes in Ca2+ current properties; transfection of mutant Cav3.2 in H295R-S2 cells increases aldosterone production and expression of steroidogenic enzymes after K+ stimulation. Whole-cell patch clamp of mutant channels in HEK cells, aldosterone production assay (ELISA), gene expression in adrenocortical cells EBioMedicine High 27729216
2016 CACNA1H M1549V expressed in HAC15 adrenocortical cells increases aldosterone production 7-fold and CYP11B2 expression; the T-type channel blocker mibefradil completely abrogates both effects, directly linking gain-of-function Cav3.2 activity to autonomous aldosterone production. Heterologous expression in HAC15 cells, aldosterone ELISA, real-time PCR for CYP11B2, pharmacological inhibition with mibefradil Endocrinology High 27258646
2017 Calnexin, an ER integral membrane protein, interacts with the III-IV linker region of Cav3.2 to modulate channel sorting to the cell surface; the GAERS missense mutation R1584P in the III-IV linker disrupts the Cav3.2/calnexin interaction, resulting in increased Cav3.2 surface expression and elevated calcium influx. Co-immunoprecipitation, surface biotinylation, whole-cell patch clamp, recombinant channel expression Scientific reports High 28912545
2013 Egr1 binds directly to the Cav3.2 promoter region 41-81 bp upstream of the TSS following transverse aortic banding (pressure overload); Egr1 knockdown prevents phenylephrine-induced Cav3.2 upregulation and cardiac hypertrophy, while Cav3.2 overexpression rescues the hypertrophic response in Egr1-knockdown cells. ChIP, EMSA, in vivo cardiac gene transfer with reporter constructs, siRNA knockdown, neonatal rat ventricular myocyte hypertrophy assay Cardiovascular research High 23929524
2013 Calcineurin physically interacts with Cav3.2; Ca2+ and calmodulin modulate this interaction. Calcineurin binding to Cav3.2 decreases calcineurin phosphatase activity and reduces Cav3.2 current density. A cell-permeable peptide mimicking the calcineurin-binding site of Cav3.2 reduces phenylephrine-induced cardiac hypertrophy. Co-immunoprecipitation, patch clamp electrophysiology, calcineurin phosphatase activity assay, cell-permeable peptide in neonatal cardiac myocytes FEBS letters High 23669360
2015 Cav3.2 is selectively expressed in Aδ- and C-low-threshold mechanoreceptors (LTMRs) innervating hair follicles; C-LTMR-specific Cav3.2 knockout reveals that Cav3.2 regulates light-touch perception, noxious mechanical/cold/chemical sensations, and is essential for allodynic symptoms of neuropathic pain. Knockin/flox mouse expressing Cav3.2-GFP fusion, C-LTMR-specific conditional knockout, behavioral sensory testing, confocal imaging of fiber trajectories Cell reports High 25600872
2015 CaV3.2 channels preferentially incorporate into synapses and control NMDA receptor-mediated transmission in an activity-dependent manner by local calcium influx. Expression of the CAE-linked hCaV3.2(C456S) mutant (higher open probability) enhances glutamatergic transmission and induces 2-4 Hz spike-wave discharges (absence-like epilepsy) in rats when expressed in cortex. Electrophysiological recordings at rat central synapses, in vivo cortical expression of mutant channels, EEG recordings, AMPA-R and NMDA-R antagonists Genes & development High 26220996
2009 The GAERS Cacna1h R1584P (gcm) missense mutation requires the presence of exon 25 to produce gain-of-function effects (faster recovery from inactivation, greater charge transference during high-frequency bursts); without exon 25, the mutation has no significant functional effect, demonstrating splice-variant-dependent epistasis. Site-directed mutagenesis of splice variants (with/without exon 25), whole-cell patch clamp in transfected cells, genetic segregation analysis in GAERS×Brown Norway F2 cross The Journal of neuroscience High 19144837
2013 C456S Cav3.2 epilepsy mutant channels increase neuronal excitability by raising spontaneous firing and lowering burst-firing threshold; the I-II loop region increases channel surface expression without altering dendritic distribution; C456S also promotes dendritic growth via Ca2+-regulated transcriptional changes, all reversed by ethosuximide or TTA-P2. Recombinant channel expression in cultured neurons, whole-cell patch clamp, immunocytochemistry, dendritic morphometry, transactivator trap (CaRE) assay, pharmacological reversal The Journal of physiology High 24277868
2010 Nitrous oxide selectively inhibits Cav3.2 T-type channels via a free radical mechanism: H191 on the extracellular face of Cav3.2 participates in a metal-binding site that generates reactive oxygen species in the presence of N2O, causing localized oxidation of H191. Cav3.2-null mice show reduced N2O analgesia in formalin-induced pain. Site-directed mutagenesis (H191), metal chelators, catalase and SOD/catalase mimetics, patch clamp, Cav3.2 knockout mouse behavioral assays The Journal of physiology High 21059758
2014 H2S selectively inhibits Cav3.2 (not Cav3.1 or Cav3.3) via the extracellular residue H191; chelation of Zn2+ prevents and reverses H2S inhibition, suggesting H2S increases the affinity of the channel for extracellular Zn2+ binding at the H191 site. Whole-cell patch clamp of heterologously expressed Cav3 isoforms in HEK293 cells, Zn2+ chelator (TPEN), native DRG neuron recordings, H191 mutant analysis FASEB journal High 25183670
2013 Carbon monoxide (CO, derived from HO-1) inhibits Cav3.2 T-type channels via an extracellular redox-sensitive site; thioredoxin (Trx) tonically maintains Cav3.2 channel activity at this site. Trx depletion reduces Cav3.2 currents and diminishes CO sensitivity. Cav3.1 and Cav3.3 are unaffected. Patch clamp in HEK293 cells expressing Cav3.1-3.3, CORM-2 application, auranofin (Trx depletion), native NG108-15 and DRG neuron recordings FASEB journal High 23671274
2015 CaV3.2 channels in resistance arteries restrain myogenic constriction through a CaV3.2→ryanodine receptor→BKCa negative feedback axis: genetic deletion of CaV3.2 enhances myogenic tone, reduces spontaneous transient outward K+ currents (BKCa activity), and abolishes Ca2+ sparks normally evoked by CaV3.2 activity. CaV3.2 knockout mice, pressurized vessel myography, patch clamp electrophysiology (BKCa STOCs), Fluo-4 Ca2+ spark imaging in en face arteries Arteriosclerosis, thrombosis, and vascular biology High 26069238
2011 Presynaptic HCN1 channels colocalize with Cav3.2 at active zones of axon terminals onto entorhinal cortical layer III pyramidal neurons; HCN channels suppress glutamate release by inhibiting presynaptic Cav3.2 T-type Ca2+ channel activity. Electron microscopy (immunogold colocalization), electrophysiology, pharmacological dissection, HCN1 knockout mice Nature neuroscience High 21358644
2021 MTF1 directly activates Cacna1h transcription in COCH neurons of ventral CA3 hippocampus; this MTF1-Cacna1h axis enables burst firing in COCH neurons and drives social-stress-induced anxiety-like behaviors via synapses onto GABAergic neurons in the lateral septum. Genetic targeting of COCH neurons, ChIP/transcriptional assays for MTF1-Cacna1h, optogenetics, electrophysiology, behavioral tests Cell reports Medium 34965426
2019 SUMOylation of USP5 at lysine K113 (via SUMO2/3) reduces USP5 affinity for Cav3.2; peripheral nerve injury decreases USP5 SUMOylation in DRG, thereby increasing USP5-Cav3.2 binding and Cav3.2 channel activity. Co-immunoprecipitation of Cav3.2 with USP5 mutants (K113R), site-directed mutagenesis, expression in tsA-201 cells, immunoblot of endogenous DRG proteins Molecular brain Medium 31455361
2017 Interleukin-1β administration increases USP5-Cav3.2 interaction in spinal dorsal horn (by Co-IP); disruption of this interaction with Tat peptides suppresses IL-1β-induced nocifensive responses, identifying IL-1β as an upstream trigger for USP5-Cav3.2 upregulation in the pain pathway. Co-immunoprecipitation from spinal tissue, intrathecal IL-1β administration, Tat peptide delivery, DRG neuron cultures, behavioral assays Molecular pain Medium 28741432
2005 In rat chromaffin cells, chronic cAMP exposure recruits Cav3.2 (α1H) T-type channels via an Epac-mediated pathway; the newly recruited T-type channels support 'low-threshold exocytosis' evoked at potentials as low as −50 mV, an effect blocked by 50 µM Ni2+ (selective T-type blocker at this concentration). RT-PCR (isoform identification), capacitance measurements of exocytosis, Ni2+ pharmacology, patch clamp, chronic cAMP treatment of rat chromaffin cells Biophysical journal Medium 16361341
2013 BK channels and Cav3.2 form macromolecular complexes in LNCaP prostate cancer cells (demonstrated by Co-IP); BK channels set resting membrane potential at ~-40 mV, promoting constitutive Ca2+ entry through Cav3.2, which together drive cell proliferation. Single-channel recording, confocal imaging, co-immunoprecipitation, siRNA knockdown, flow cytometry (cell cycle), cell survival assay Biology open Medium 24143281
2010 ACTH induces Cav3.2 current and CACNA1H mRNA in adrenal zona fasciculata cells by mechanisms only partly dependent on cAMP; cAMP analogs increase CACNA1H mRNA but not Ca2+ current; 8CPT-cAMP metabolites (including 8CPT-adenosine) increase both mRNA and current, revealing a cAMP-independent pathway for Cav3.2 upregulation by ACTH. Northern blot, whole-cell patch clamp in bovine AZF cells, pharmacological cAMP analog panel The Journal of biological chemistry Medium 20424171
2009 MCP-1 directly inhibits Cav3.2 channels with nanomolar affinity independently of CCR2 receptor activation; this direct inhibition is sensitive to divalent metal ion chelator DTPA, suggesting metal ions as a cofactor. MCP-1 also inhibits native T-type currents in acutely dissociated DRG neurons. Whole-cell patch clamp of Cav3 isoforms in tsA-201 cells, heat denaturation controls, DTPA chelation, DRG neuron recordings Molecular pharmacology Medium 19864434
2018 Melatonin inhibits Cav3.2 T-type channels in trigeminal ganglion neurons via MT2 receptor → Gαo (pertussis toxin-sensitive) → Gβγ → novel PKCη signaling; PKCη antagonism or knockdown prevents melatonin effects; MT2 activation selectively inhibits Cav3.2 but not Cav3.1 or Cav3.3 in heterologous expression. Patch clamp in TG neurons and heterologous expression, co-IP of MT2/Gαo, QEHA peptide, shRNA knockdown of Gαo and PKCη, behavioral inflammatory pain model Journal of pineal research Medium 29437250
2021 Neuromedin B receptor (NmbR) selectively potentiates Cav3.2 (not Cav3.1 or Cav3.3) currents in trigeminal ganglion neurons via Gq-coupled Gβγ → AMPK → PKA signaling cascade; AMPK inhibition prevents Nmb-induced increase in PKA activity; Cav3.2 siRNA knockdown abolishes NmbR-driven pain hypersensitivity in vivo. Patch clamp in TG neurons and heterologous system, QEHA peptide, shRNA of Gβ, AMPK/PKA inhibitors, phospho-AMPK western blot, behavioral inflammatory pain model with Cav3.2 siRNA Theranostics Medium 34646374
2013 CaV3.2 channel opening during ischemia (OGD) contributes Ca2+ that is transmitted to mitochondria, causing deleterious mitochondrial Ca2+ overload; Cav3.2 overexpression worsens ischemic toxicity and mitochondrial Ca2+ loading, while Ni2+ block and Cav3.1/Cav3.2 siRNA are protective. Ca2+ imaging (cytosolic and mitochondrial) in PC12 cells, Cav3.2 overexpression and siRNA knockdown, Ni2+ pharmacology, ATP measurement, cell death assay The Journal of biological chemistry Medium 23508951
2007 Cav3.2 T-type Ca2+ current is the molecular determinant of GABA-induced excitability in a subset of adult sensory neurons: Cav3.2-null mice lack T-type current and show no GABAA receptor-induced action potential firing or intracellular Ca2+ increase in this neuron subset. Cav3.2 knockout mice, patch clamp, intracellular Ca2+ imaging, GABAA receptor pharmacology Molecular and cellular neurosciences Medium 17716912
2014 CaV3.2 channels in carotid body glomus cells mediate the H2S-dependent hypoxic Ca2+ response: CaV3.2 knockout mice show markedly attenuated hypoxia-evoked intracellular Ca2+ increases, catecholamine secretion, and sensory nerve excitation; NaHS (H2S donor) effects are also markedly reduced in Cacna1h-/- mice. Cav3.2 knockout mice, intracellular Ca2+ imaging in glomus cells, catecholamine secretion assay, carotid body sensory nerve recording, pharmacological T-type blockers American journal of physiology. Cell physiology Medium 25377087
2018 Cav3.2 channels at the axon initial segment of mature dentate granule cells are responsible for burst firing: Cav3.2 knockout mice fire tonic spikes instead of bursts, exhibit impaired synaptic plasticity, and show reduced dentate-to-CA3 communication. Cav3.2 knockout mice, patch clamp electrophysiology in granule cells, synaptic plasticity recordings, axon initial segment localization Cerebral cortex Medium 29790938
2004 Cav3.2 is the predominant T-type Ca2+ channel subtype expressed in embryonic mouse heart (E9.5 and E18), as determined by quantitative PCR; Cav3.2 mRNA predominates over Cav3.1 during embryonic period, then switches to Cav3.1 predominance in adulthood; T-type currents in embryonic ventricular myocytes are sensitive to low Ni2+ concentrations (IC50 26-31 µM), consistent with Cav3.2. Quantitative PCR, whole-cell patch clamp with Ni2+ pharmacology in acutely isolated mouse ventricular myocytes at developmental stages American journal of physiology. Heart and circulatory physiology Medium 14988077
2013 Immunoelectron microscopy demonstrates that Cav3.2 protein is expressed in soma and peripheral axons of small-diameter (nociceptive, IB4+, CGRP+) DRG neurons and in unmyelinated sciatic nerve fibers, as well as in peripheral nerve endings of hind-paw skin. Polyclonal Cav3.2 antibody, confocal immunofluorescence, electron microscopy with immunogold labeling, co-localization with nociceptor markers Neuroscience Medium 23867767
2013 S-nitrosothiols (SNOs such as GSNO) inhibit CaV3.2 T-type channels in DRG neurons by acting on putative extracellular cysteine thiol residues in repeats I and II; a quadruple Cys-Ala mutant at these sites abolishes GSNO inhibition without affecting voltage dependence. Site-directed mutagenesis (quadruple Cys-Ala in repeats I/II), patch clamp in DRG neurons and HEK cells, N-ethylmaleimide pretreatment, guanylyl cyclase inhibitor controls Molecular neurobiology Medium 23813099
2009 H2S (NaHS) activates or sensitizes Cav3.2 T-type channels expressed in primary afferents and spinal nociceptive neurons, causing hyperalgesia; antisense knockdown of Cav3.2 protein in DRG and spinal cord attenuates both intrathecal and intraplantar NaHS-induced hyperalgesia, while zinc chloride (preferential Cav3.2 blocker) and mibefradil reproduce this effect. Antisense oligodeoxynucleotide knockdown, Western blot for Cav3.2 protein, paw pressure nociceptive threshold, pharmacological (zinc chloride, mibefradil) Pain Medium 19167819
2022 miR-32-5p directly targets Cav3.2 mRNA in trigeminal ganglion neurons; nerve injury causes histone methylation (H3K9me2, H3K27me3) at the miR-32-5p promoter, suppressing miR-32-5p and de-repressing Cav3.2 protein and T-type currents to drive trigeminal neuropathic pain. High-throughput miRNA sequencing, qPCR, histone methyltransferase inhibitors, lentiviral miR-32-5p overexpression, Western blot, patch clamp, behavioral pain assays PNAS Medium 35353623
2020 A somatic CACNA1H I1430T mutation in aldosterone-producing adenoma, when expressed in HAC15 cells via inducible system, increases CYP11B2 mRNA and aldosterone production, supporting its role as a driver of autonomous aldosterone secretion. CYP11B2-guided exome sequencing, doxycycline-inducible CACNA1H I1430T expression in HAC15 cells, CYP11B2 qPCR, aldosterone ELISA Hypertension Medium 31983310
2021 Cacna1h knockin (M1549V) mice have increased aldosterone:renin ratios, elevated adrenal Cyp11b2 expression (not suppressed by high salt), and 8 mmHg higher systolic blood pressure than wild-type; adrenal glomerulosa cells from knockin mice show increased baseline and peak intracellular Ca2+ concentrations, establishing elevated intracellular Ca2+ as the mechanistic link between gain-of-function Cav3.2 and aldosterone overproduction. CRISPR/Cas9 knockin and knockout mice, blood pressure telemetry, aldosterone/renin assay, adrenal slice Ca2+ imaging (zona glomerulosa), qPCR PNAS High 33879608

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2004 Silencing of the Cav3.2 T-type calcium channel gene in sensory neurons demonstrates its major role in nociception. The EMBO journal 366 15616581
2003 Association between genetic variation of CACNA1H and childhood absence epilepsy. Annals of neurology 286 12891677
2015 Recurrent gain of function mutation in calcium channel CACNA1H causes early-onset hypertension with primary aldosteronism. eLife 259 25907736
2014 The deubiquitinating enzyme USP5 modulates neuropathic and inflammatory pain by enhancing Cav3.2 channel activity. Neuron 214 25189210
2008 Transcriptional upregulation of Cav3.2 mediates epileptogenesis in the pilocarpine model of epilepsy. The Journal of neuroscience : the official journal of the Society for Neuroscience 172 19052226
2006 CACNA1H mutations in autism spectrum disorders. The Journal of biological chemistry 170 16754686
2017 Dorsal root ganglion neurons become hyperexcitable and increase expression of voltage-gated T-type calcium channels (Cav3.2) in paclitaxel-induced peripheral neuropathy. Pain 164 27902567
2015 The Low-Threshold Calcium Channel Cav3.2 Determines Low-Threshold Mechanoreceptor Function. Cell reports 162 25600872
2007 Extended spectrum of idiopathic generalized epilepsies associated with CACNA1H functional variants. Annals of neurology 151 17696120
2009 A Cav3.2 T-type calcium channel point mutation has splice-variant-specific effects on function and segregates with seizure expression in a polygenic rat model of absence epilepsy. The Journal of neuroscience : the official journal of the Society for Neuroscience 148 19144837
2005 Functional characterization and neuronal modeling of the effects of childhood absence epilepsy variants of CACNA1H, a T-type calcium channel. The Journal of neuroscience : the official journal of the Society for Neuroscience 143 15888660
2004 Gating effects of mutations in the Cav3.2 T-type calcium channel associated with childhood absence epilepsy. The Journal of biological chemistry 142 14729682
2002 Overexpression of an alpha 1H (Cav3.2) T-type calcium channel during neuroendocrine differentiation of human prostate cancer cells. The Journal of biological chemistry 142 11799114
2011 Presynaptic HCN1 channels regulate Cav3.2 activity and neurotransmission at select cortical synapses. Nature neuroscience 139 21358644
2016 CACNA1H Mutations Are Associated With Different Forms of Primary Aldosteronism. EBioMedicine 122 27729216
2009 Hyperalgesia induced by spinal and peripheral hydrogen sulfide: evidence for involvement of Cav3.2 T-type calcium channels. Pain 119 19167819
2013 Surface expression and function of Cav3.2 T-type calcium channels are controlled by asparagine-linked glycosylation. Pflugers Archiv : European journal of physiology 91 23503728
2005 Effects of Cav3.2 channel mutations linked to idiopathic generalized epilepsy. Annals of neurology 88 15852375
2020 Somatic CACNA1H Mutation As a Cause of Aldosterone-Producing Adenoma. Hypertension (Dallas, Tex. : 1979) 85 31983310
2004 Cav3.2 subunit underlies the functional T-type Ca2+ channel in murine hearts during the embryonic period. American journal of physiology. Heart and circulatory physiology 82 14988077
2008 Molecular pharmacology of human Cav3.2 T-type Ca2+ channels: block by antihypertensives, antiarrhythmics, and their analogs. The Journal of pharmacology and experimental therapeutics 77 18974361
2006 CaV3.2 is the major molecular substrate for redox regulation of T-type Ca2+ channels in the rat and mouse thalamus. The Journal of physiology 77 16644797
2013 Chronic hypoxia selectively enhances L- and T-type voltage-dependent Ca2+ channel activity in pulmonary artery by upregulating Cav1.2 and Cav3.2. American journal of physiology. Lung cellular and molecular physiology 74 23686856
2006 A profile of alternative RNA splicing and transcript variation of CACNA1H, a human T-channel gene candidate for idiopathic generalized epilepsies. Human molecular genetics 73 16565161
2013 Immunohistological demonstration of CaV3.2 T-type voltage-gated calcium channel expression in soma of dorsal root ganglion neurons and peripheral axons of rat and mouse. Neuroscience 71 23867767
2012 Hydrogen sulfide-induced mechanical hyperalgesia and allodynia require activation of both Cav3.2 and TRPA1 channels in mice. British journal of pharmacology 71 22300342
2021 Targeting T-type/CaV3.2 channels for chronic pain. Translational research : the journal of laboratory and clinical medicine 69 33422652
2013 Mechanisms by which a CACNA1H mutation in epilepsy patients increases seizure susceptibility. The Journal of physiology 69 24277868
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
2005 Expression of voltage sensitive calcium channel (VSCC) L-type Cav1.2 (alpha1C) and T-type Cav3.2 (alpha1H) subunits during mouse bone development. Developmental dynamics : an official publication of the American Association of Anatomists 67 16059921
2019 Ca2+ and CACNA1H mediate targeted suppression of breast cancer brain metastasis by AM RF EMF. EBioMedicine 65 31129098
2012 Transcriptional regulation of T-type calcium channel CaV3.2: bi-directionality by early growth response 1 (Egr1) and repressor element 1 (RE-1) protein-silencing transcription factor (REST). The Journal of biological chemistry 62 22431737
2014 T-type calcium channel Cav3.2 deficient mice show elevated anxiety, impaired memory and reduced sensitivity to psychostimulants. Frontiers in behavioral neuroscience 61 24672455
2008 Activation of corticotropin-releasing factor receptor 1 selectively inhibits CaV3.2 T-type calcium channels. Molecular pharmacology 59 18292205
2014 Cav3.2 T-type calcium channel is required for the NFAT-dependent Sox9 expression in tracheal cartilage. Proceedings of the National Academy of Sciences of the United States of America 58 24778262
2013 Specific functioning of Cav3.2 T-type calcium and TRPV1 channels under different types of STZ-diabetic neuropathy. Biochimica et biophysica acta 56 23376589
2016 CACNA1H(M1549V) Mutant Calcium Channel Causes Autonomous Aldosterone Production in HAC15 Cells and Is Inhibited by Mibefradil. Endocrinology 53 27258646
2006 Augmentation of Cav3.2 T-type calcium channel activity by cAMP-dependent protein kinase A. The Journal of pharmacology and experimental therapeutics 53 16569752
2014 Endogenous and exogenous hydrogen sulfide facilitates T-type calcium channel currents in Cav3.2-expressing HEK293 cells. Biochemical and biophysical research communications 49 24508802
2015 Phosphorylation of the Cav3.2 T-type calcium channel directly regulates its gating properties. Proceedings of the National Academy of Sciences of the United States of America 47 26483470
2015 Expression and Regulation of Cav3.2 T-Type Calcium Channels during Inflammatory Hyperalgesia in Mouse Dorsal Root Ganglion Neurons. PloS one 45 25974104
2017 Identification of interleukin-1 beta as a key mediator in the upregulation of Cav3.2-USP5 interactions in the pain pathway. Molecular pain 44 28741432
2015 CaV3.2 calcium channels control NMDA receptor-mediated transmission: a new mechanism for absence epilepsy. Genes & development 42 26220996
2016 Suppression of Sleep Spindle Rhythmogenesis in Mice with Deletion of CaV3.2 and CaV3.3 T-type Ca(2+) Channels. Sleep 41 26612388
2015 Genetic ablation of CaV3.2 channels enhances the arterial myogenic response by modulating the RyR-BKCa axis. Arteriosclerosis, thrombosis, and vascular biology 41 26069238
2005 Low-threshold exocytosis induced by cAMP-recruited CaV3.2 (alpha1H) channels in rat chromaffin cells. Biophysical journal 41 16361341
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
2014 Hydrogen sulfide inhibits Cav3.2 T-type Ca2+ channels. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 38 25183670
2006 New variants in the CACNA1H gene identified in childhood absence epilepsy. Neuroscience letters 37 16905256
2022 Histone methylation-mediated microRNA-32-5p down-regulation in sensory neurons regulates pain behaviors via targeting Cav3.2 channels. Proceedings of the National Academy of Sciences of the United States of America 36 35353623
2013 Functional coupling between large-conductance potassium channels and Cav3.2 voltage-dependent calcium channels participates in prostate cancer cell growth. Biology open 36 24143281
2009 Protein kinase A activity controls the regulation of T-type CaV3.2 channels by Gbetagamma dimers. The Journal of biological chemistry 36 19131331
2019 Inhibition of CACNA1H attenuates doxorubicin-induced acute cardiotoxicity by affecting endoplasmic reticulum stress. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 35 31580970
2016 CACNA1H missense mutations associated with amyotrophic lateral sclerosis alter Cav3.2 T-type calcium channel activity and reticular thalamic neuron firing. Channels (Austin, Tex.) 35 27331657
2009 Structural determinants of the high affinity extracellular zinc binding site on Cav3.2 T-type calcium channels. The Journal of biological chemistry 35 19940152
2015 Hydrogen sulfide-induced itch requires activation of Cav3.2 T-type calcium channel in mice. Scientific reports 34 26602811
2019 Nerve injury elevates functional Cav3.2 channels in superficial spinal dorsal horn. Molecular pain 33 30803310
2016 The voltage gated Ca(2+)-channel Cav3.2 and therapeutic responses in breast cancer. Cancer cell international 33 27034617
2013 Carbon monoxide inhibition of Cav3.2 T-type Ca2+ channels reveals tonic modulation by thioredoxin. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 33 23671274
2012 CACNA1H antibodies associated with headache with neurological deficits and cerebrospinal fluid lymphocytosis (HaNDL). Cephalalgia : an international journal of headache 33 23111027
2014 Roles of Cav3.2 and TRPA1 channels targeted by hydrogen sulfide in pancreatic nociceptive processing in mice with or without acute pancreatitis. Journal of neuroscience research 32 25267397
2014 NMP-7 inhibits chronic inflammatory and neuropathic pain via block of Cav3.2 T-type calcium channels and activation of CB2 receptors. Molecular pain 32 25481027
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
2014 Epigallocatechin-3-gallate elicits Ca2+ spike in MCF-7 breast cancer cells: essential role of Cav3.2 channels. Cell calcium 31 25260713
2010 Free radical signalling underlies inhibition of CaV3.2 T-type calcium channels by nitrous oxide in the pain pathway. The Journal of physiology 31 21059758
2016 Modulation of Cav3.2 T-type calcium channel permeability by asparagine-linked glycosylation. Channels (Austin, Tex.) 30 26745591
2015 Functional upregulation of the H2S/Cav3.2 channel pathway accelerates secretory function in neuroendocrine-differentiated human prostate cancer cells. Biochemical pharmacology 30 26256074
2009 Role of the T-type calcium channel CaV3.2 in the chronotropic action of corticosteroids in isolated rat ventricular myocytes. Endocrinology 29 19443576
2017 The Cacna1h mutation in the GAERS model of absence epilepsy enhances T-type Ca2+ currents by altering calnexin-dependent trafficking of Cav3.2 channels. Scientific reports 28 28912545
2006 Common polymorphisms in the CACNA1H gene associated with childhood absence epilepsy in Chinese Han population. Annals of human genetics 28 17156077
2003 The gating and conductance properties of Cav3.2 low-voltage-activated T-type calcium channels. The Japanese journal of physiology 28 14529577
2021 Enhanced Ca2+ signaling, mild primary aldosteronism, and hypertension in a familial hyperaldosteronism mouse model (Cacna1h ). Proceedings of the National Academy of Sciences of the United States of America 26 33879608
2018 The Low-Threshold Calcium Channel Cav3.2 Mediates Burst Firing of Mature Dentate Granule Cells. Cerebral cortex (New York, N.Y. : 1991) 26 29790938
2019 SUMOylation regulates USP5-Cav3.2 calcium channel interactions. Molecular brain 25 31455361
2017 Functional variants in HCN4 and CACNA1H may contribute to genetic generalized epilepsy. Epilepsia open 25 29588962
2015 Association study between polymorphisms in the CACNA1A, CACNA1C, and CACNA1H genes and drug-resistant epilepsy in the Chinese Han population. Seizure 25 26216687
2019 Compound heterozygous CACNA1H mutations associated with severe congenital amyotrophy. Channels (Austin, Tex.) 24 31070086
2018 Melatonin-mediated inhibition of Cav3.2 T-type Ca2+ channels induces sensory neuronal hypoexcitability through the novel protein kinase C-eta isoform. Journal of pineal research 23 29437250
2022 A Synthetically Accessible Small-Molecule Inhibitor of USP5-Cav3.2 Calcium Channel Interactions with Analgesic Properties. ACS chemical neuroscience 21 35113527
2021 Neuromedin B receptor stimulation of Cav3.2 T-type Ca2+ channels in primary sensory neurons mediates peripheral pain hypersensitivity. Theranostics 21 34646374
2015 Two heterozygous Cav3.2 channel mutations in a pediatric chronic pain patient: recording condition-dependent biophysical effects. Pflugers Archiv : European journal of physiology 21 26706850
2007 The Cav3.2/alpha1H T-type Ca2+ current is a molecular determinant of excitatory effects of GABA in adult sensory neurons. Molecular and cellular neurosciences 21 17716912
2023 Cav3.2 channel regulates cerebral ischemia/reperfusion injury: a promising target for intervention. Neural regeneration research 20 38526284
2021 A circuit of COCH neurons encodes social-stress-induced anxiety via MTF1 activation of Cacna1h. Cell reports 20 34965426
2020 CACNA1H variants are not a cause of monogenic epilepsy. Human mutation 20 32227660
2016 Colocalization of insulin-like growth factor-1 receptor and T type Cav3.2 channel in dorsal root ganglia in chronic inflammatory pain mouse model. Neuroreport 20 27213932
2013 Mitochondrial Ca2+ uptake from plasma membrane Cav3.2 protein channels contributes to ischemic toxicity in PC12 cells. The Journal of biological chemistry 20 23508951
2009 CCR2 receptor ligands inhibit Cav3.2 T-type calcium channels. Molecular pharmacology 20 19864434
2005 Pathophysiological significance of T-type Ca2+ channels: transcriptional regulation of T-type Ca2+ channel--regulation of CACNA1H by neuron-restrictive silencer factor. Journal of pharmacological sciences 20 16272789
2013 Physical interaction between calcineurin and Cav3.2 T-type Ca2+ channel modulates their functions. FEBS letters 19 23669360
2020 A rare CACNA1H variant associated with amyotrophic lateral sclerosis causes complete loss of Cav3.2 T-type channel activity. Molecular brain 18 32143681
2020 CACNA1H downregulation induces skeletal muscle atrophy involving endoplasmic reticulum stress activation and autophagy flux blockade. Cell death & disease 18 32332705
2018 Disrupting USP5/Cav3.2 interactions protects female mice from mechanical hypersensitivity during peripheral inflammation. Molecular brain 18 30340616
2014 CaV3.2 T-type Ca²⁺ channels in H₂S-mediated hypoxic response of the carotid body. American journal of physiology. Cell physiology 18 25377087
2013 Early growth response 1 is an early signal inducing Cav3.2 T-type calcium channels during cardiac hypertrophy. Cardiovascular research 18 23929524
2010 ACTH induces Cav3.2 current and mRNA by cAMP-dependent and cAMP-independent mechanisms. The Journal of biological chemistry 18 20424171
2013 Redox mechanism of S-nitrosothiol modulation of neuronal CaV3.2 T-type calcium channels. Molecular neurobiology 17 23813099
2010 Fast, repetitive light-activation of CaV3.2 using channelrhodopsin 2. Channels (Austin, Tex.) 17 20714225
2009 Protein kinase C-mediated inhibition of recombinant T-type Cav3.2 channels by neurokinin 1 receptors. Molecular pharmacology 17 19805509
2009 G protein-mediated inhibition of Cav3.2 T-type channels revisited. Molecular pharmacology 17 19903827

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