Affinage

CACNA1D

Voltage-dependent L-type calcium channel subunit alpha-1D · UniProt Q01668

Length
2161 aa
Mass
245.1 kDa
Annotated
2026-04-28
100 papers in source corpus 37 papers cited in narrative 37 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CACNA1D encodes the pore-forming α1D subunit of the CaV1.3 L-type voltage-gated Ca²⁺ channel, which activates at uniquely negative membrane potentials and is essential for cardiac pacemaking, auditory hair cell synaptic transmission, and neuroendocrine signaling. Channel gating is tuned by C-terminal alternative splicing that controls a modulatory domain (CTM) regulating voltage-sensor–to–pore coupling (PMID:18482979, PMID:24703308), by ADAR2-mediated RNA editing at the IQ domain that modulates calmodulin-dependent inactivation (PMID:24120865, PMID:29733375), and by phosphorylation through PKA (potentiating), PKC-βII/ε (inhibitory at N-terminal S81), and CaMKII (facilitating at EF-hand S1486) (PMID:15615842, PMID:16973824, PMID:16763033). CaV1.3 is organized at presynaptic ribbon active zones and postsynaptic densities through scaffolding interactions with Shank, harmonin, RIM2α/β, and the auxiliary α₂δ2 subunit, which together govern channel clustering, surface stability, trans-synaptic alignment, and coupling to vesicle release and RyR2-mediated Ca²⁺-induced Ca²⁺ release (PMID:15689539, PMID:21822269, PMID:26034270, PMID:27798183, PMID:17823125). Loss-of-function mutations cause SANDD syndrome (sinoatrial node dysfunction and deafness) (PMID:21131953), while gain-of-function mutations in S6 pore-lining segments cause aldosterone-producing adenomas, primary aldosteronism, and autism spectrum disorder with epilepsy (PMID:23913001, PMID:25620733, PMID:28472301).

Mechanistic history

Synthesis pass · year-by-year structured walk · 21 steps
  1. 2001 High

    Establishing that CaV1.3 activates at uniquely negative voltages distinguished it from CaV1.2 and explained how L-type channels could operate at subthreshold potentials in pacemaker and sensory cells.

    Evidence Whole-cell patch-clamp and radioligand binding of exon 8A splice variant in tsA-201 cells

    PMID:11285265

    Open questions at the time
    • Molecular basis of negative activation threshold not yet mapped to specific structural domains
    • In vivo splice variant distribution unknown
  2. 2001 Medium

    Demonstrating PKC-dependent stimulation of CaV1.3 by Gi/Go-coupled GPCRs revealed a GPCR modulatory pathway distinct from CaV2.2 inhibition.

    Evidence Pharmacological dissection in Xenopus oocyte expression system

    PMID:11435619

    Open questions at the time
    • PKC phosphorylation site not identified in this study
    • Not confirmed in native neuroendocrine cells
  3. 2003 High

    Genetic knockout established that CaV1.3 is essential for both cardiac pacemaker diastolic depolarization and cochlear inner hair cell exocytosis, defining its two principal physiological roles.

    Evidence CaV1.3−/− mice with patch-clamp of SAN cells and IHC capacitance measurements

    PMID:12700358 PMID:14645476

    Open questions at the time
    • Molecular identity of CaV1.3 coupling partners at IHC active zones unknown
    • Contribution of other channel types to residual pacemaking not fully resolved
  4. 2005 High

    Quantification of CaV1.3 clustering at ribbon active zones and demonstration of nanodomain Ca²⁺ coupling to vesicle release established the biophysical framework for how few channels drive transmitter release at auditory synapses.

    Evidence Nonstationary fluctuation analysis, immunohistochemistry, and capacitance recordings in IHCs

    PMID:16354915

    Open questions at the time
    • Identity of the molecular tether linking CaV1.3 to release sites unknown
    • Single-channel properties in native IHCs not directly measured
  5. 2005 High

    Identification of Shank as a PDZ-domain scaffold that clusters CaV1.3 at synapses and enables GPCR modulation resolved how CaV1.3 is positioned in postsynaptic signaling complexes.

    Evidence Yeast two-hybrid, pull-down, dominant-negative peptides in hippocampal neurons; D2/M1 receptor modulation requiring Shank–Homer in striatal neurons from CaV1.3 KO mice

    PMID:15689539 PMID:15689540

    Open questions at the time
    • Shank interaction stoichiometry unknown
    • Whether Shank mediates CaV1.3 clustering at all synapse types untested
  6. 2006 High

    Mapping specific kinase phosphorylation sites—CaMKII at S1486 (facilitating) and PKC-βII/ε at S81 (inhibitory)—and PKA-dependent potentiation defined the phosphoregulatory landscape of CaV1.3.

    Evidence Site-directed mutagenesis, phosphomimetic constructs, isoform-specific pharmacology, and patch-clamp in tsA-201 and cortical neurons

    PMID:15615842 PMID:16763033 PMID:16973824

    Open questions at the time
    • PKA phosphorylation site on α1D not identified
    • In vivo relevance of each phosphorylation event not established
  7. 2007 High

    Discovery that CaBP1 suppresses Ca²⁺-dependent inactivation at IHC ribbon synapses and that CaV1.3 physically couples to RyR2 for voltage-triggered intracellular Ca²⁺ release expanded the Ca²⁺-sensing and amplification machinery associated with CaV1.3.

    Evidence Co-immunoprecipitation, heterologous electrophysiology, yeast two-hybrid, siRNA knockdown in hippocampal neurons, IHC immunolocalization

    PMID:17823125 PMID:17947313

    Open questions at the time
    • CaBP1 binding site on CaV1.3 not mapped at residue level
    • Stoichiometry of CaV1.3–RyR2 coupling complex unknown
  8. 2008 High

    Identification of the C-terminal modulatory domain (CTM) as an intramolecular brake that weakens calmodulin binding and shifts activation positive revealed how alternative C-terminal splicing tunes CaV1.3 gating.

    Evidence FRET, truncation constructs, and patch-clamp of long vs. short splice variants in HEK-293 cells

    PMID:18482979

    Open questions at the time
    • CTM structural basis at atomic level unresolved
    • Relative expression of long vs. short splice variants across tissues not systematically mapped
  9. 2008 High

    Demonstration that otoferlin C2D domain binds the CaV1.3 II–III loop in a Ca²⁺-dependent manner, disrupted by the deafness mutation L1011P, established the molecular link between the Ca²⁺ channel and the SNARE-associated release machinery at IHC synapses.

    Evidence Fusion protein pull-down with disease mutants and Ca²⁺-dependent binding assays

    PMID:19004828

    Open questions at the time
    • Functional consequence of disrupting this interaction on exocytosis not directly tested in this study
    • Whether otoferlin replaces synaptotagmin function entirely at IHC synapses not resolved
  10. 2010 High

    Discovery that SANDD syndrome results from a loss-of-function CACNA1D mutation proved CaV1.3 is indispensable for human sinoatrial pacemaking and hearing, translating mouse knockout findings to human disease.

    Evidence Positional cloning in consanguineous family, Sanger sequencing, heterologous expression of mutant channels with patch-clamp

    PMID:21131953

    Open questions at the time
    • Prevalence of CACNA1D loss-of-function variants in unexplained bradycardia or deafness not established
    • No rescue or gene therapy attempted
  11. 2010 High

    Identification of densin–CaMKII complex as required for Ca²⁺-dependent facilitation, RIM2α/β as modulators of inactivation and channel clustering, and GABABR2 as a direct binding partner expanded the macromolecular signaling complex at CaV1.3-containing synapses.

    Evidence Co-immunoprecipitation from brain, heterologous electrophysiology, co-localization in IHCs, yeast two-hybrid and GST pull-down for GABABR2

    PMID:20363327 PMID:20392935 PMID:20627102

    Open questions at the time
    • GABABR2–CaV1.3 interaction confirmed in single lab
    • Structural basis for RIM2–β-subunit interaction unresolved
  12. 2011 High

    Showing that harmonin promotes ubiquitin-dependent degradation of CaV1.3 while also enhancing voltage-dependent facilitation revealed a dual scaffolding/quality-control mechanism at IHC presynapses.

    Evidence Co-immunoprecipitation at native IHC synapse, ubiquitin assay, and electrophysiology in dfcr harmonin mutant mice

    PMID:21822269 PMID:23613530

    Open questions at the time
    • E3 ligase responsible for CaV1.3 ubiquitination not identified
    • Whether harmonin-mediated degradation is activity-dependent unknown
  13. 2013 High

    Discovery that somatic CACNA1D gain-of-function mutations in S6 segments cause aldosterone-producing adenomas established CaV1.3 as a driver of autonomous aldosterone secretion and primary aldosteronism.

    Evidence Whole-exome sequencing of adenomas, heterologous expression and patch-clamp of G403R and I770M mutants

    PMID:23913001

    Open questions at the time
    • Frequency of CACNA1D mutations across all aldosterone-producing adenomas not fully defined
    • Downstream transcriptional programs activated by mutant CaV1.3 in adrenal cells not mapped
  14. 2013 High

    Elucidation that ADAR2-mediated RNA editing at the IQ domain weakens apoCaM prebinding rather than Ca²⁺/CaM binding established a continuously tunable mechanism for CDI regulation unique to neurons.

    Evidence Patch-clamp of edited channel variants with calmodulin titration, substantia nigra neuron recordings

    PMID:24120865

    Open questions at the time
    • Editing levels across brain regions and disease states incompletely characterized
    • Whether editing and CTM splicing interact combinatorially untested
  15. 2014 High

    Biophysical demonstration that CTM controls voltage-sensor–to–pore coupling efficiency (not voltage-sensor movement itself) provided a mechanistic explanation for how C-terminal splicing shifts CaV1.3 activation threshold.

    Evidence Gating current (QON-V) vs. ionic current recordings of long and short splice variants in tsA-201 cells

    PMID:24703308

    Open questions at the time
    • Structural interaction between CTM and voltage-sensing domains not visualized
    • Whether CTM coupling mechanism is conserved across CaV1 family unknown
  16. 2014 High

    Characterization of de novo CACNA1D mutations A749G and G407R as gain-of-function in autism spectrum disorder patients linked CaV1.3 hyperactivity to neurodevelopmental disease beyond aldosteronism.

    Evidence Whole-cell patch-clamp of mutant channels in tsA-201 cells; patient genotyping

    PMID:25620733

    Open questions at the time
    • Circuit-level consequences of gain-of-function in developing brain not modeled
    • No animal model of these specific mutations
  17. 2015 High

    Conditional knockout and superresolution imaging of RIM2α at IHC active zones demonstrated that RIM proteins stabilize CaV1.3 channel number at release sites and that reduced channel number proportionally reduces exocytosis.

    Evidence Hair cell–specific RIM2α conditional KO, STED microscopy, fluctuation analysis, electron tomography

    PMID:26034270

    Open questions at the time
    • Whether RIM2 directly tethers CaV1.3 or acts through β-subunit only is unresolved
    • Role of RIM1 at IHC synapses not addressed
  18. 2016 High

    Characterization of the α₂δ2 auxiliary subunit's role in CaV1.3 surface expression, gating, and trans-synaptic alignment with postsynaptic AMPA receptor clusters revealed an organizing function beyond simple current enhancement.

    Evidence Patch-clamp, immunofluorescence, and Ca²⁺ imaging in ducky (α₂δ2-null) mouse IHCs

    PMID:27798183

    Open questions at the time
    • Mechanism of trans-synaptic signaling from presynaptic α₂δ2 to postsynaptic PSD-95/AMPA receptors not identified
    • Whether α₂δ2 similarly organizes CaV1.3 synapses in neurons unknown
  19. 2016 High

    Demonstration that CaV1.3 provides diastolic Ca²⁺ influx that triggers and synchronizes local RyR-dependent Ca²⁺ release events in SAN cells, rescuable by caffeine, refined the coupled-clock pacemaker model by defining CaV1.3 as the voltage-clock input to the Ca²⁺ clock.

    Evidence Live Ca²⁺ imaging in CaV1.3−/− and WT SAN cells with caffeine rescue

    PMID:26786159

    Open questions at the time
    • Spatial relationship between CaV1.3 and RyR clusters in SAN not resolved at nanoscale
    • Contribution of CaV1.3 splice variants to SAN pacemaking not distinguished
  20. 2018 High

    Identification of SRSF9 as the splicing factor that restricts ADAR2-mediated CaV1.3 editing to neurons (by blocking the editing-site RNA duplex in non-neuronal cells) resolved the cell-type specificity of CaV1.3 RNA editing.

    Evidence Minigene editing assay, CLIP/RIP for direct SRSF9–RNA binding, SRSF9 knockdown/overexpression

    PMID:29733375

    Open questions at the time
    • Whether SRSF9 regulation is dynamic within neurons (e.g., activity-dependent) unknown
    • Other edited sites in CaV1.3 not examined
  21. 2020 High

    Comparative analysis of gain-of-function (S652L) versus loss-of-function (S652W) mutations at the same residue established that only gain-of-function variants confer high disease risk and showed that GOF mutants can paradoxically increase DHP sensitivity, suggesting pharmacological rescue potential.

    Evidence Whole-cell patch-clamp with AP-clamp waveforms and isradipine dose-response in tsA-201 cells

    PMID:31921405

    Open questions at the time
    • In vivo efficacy of isradipine for GOF CACNA1D channelopathies not tested
    • Whether increased DHP sensitivity generalizes across GOF mutations unknown

Open questions

Synthesis pass · forward-looking unresolved questions
  • Major open questions include the atomic structure of the CaV1.3 CTM–channel body interaction, the identity of the E3 ubiquitin ligase mediating harmonin-dependent CaV1.3 degradation, the combinatorial effects of RNA editing and C-terminal splicing on native channel behavior, and whether DHP pharmacotherapy can rescue gain-of-function channelopathies in vivo.
  • No high-resolution structure of full-length CaV1.3 with CTM
  • E3 ligase for harmonin-mediated ubiquitination unidentified
  • In vivo pharmacological rescue of GOF mutations untested

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005215 transporter activity 5 GO:0140299 molecular sensor activity 2
Localization
GO:0005886 plasma membrane 5 GO:0005634 nucleus 1 GO:0005929 cilium 1
Pathway
R-HSA-162582 Signal Transduction 6 R-HSA-9709957 Sensory Perception 6 R-HSA-112316 Neuronal System 5 R-HSA-1643685 Disease 5 R-HSA-382551 Transport of small molecules 4
Partners
CACNA2D2CAMK2AGABBR2OTOFRIM2RYR2SHANK1USH1C

Evidence

Reading pass · 37 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2001 Human CaV1.3 (α1D) splice variant containing exon 8A forms L-type Ca²⁺ channels that activate at more negative voltages (threshold ~−45.7 mV) and inactivate more slowly than CaV1.2; reduced dihydropyridine sensitivity results from voltage-dependence of DHP block rather than lower binding affinity, as shown by radioligand binding and patch-clamp in tsA-201 cells. Whole-cell patch-clamp electrophysiology, radioligand binding, heterologous expression in tsA-201 cells The Journal of biological chemistry High 11285265
2001 CaV1.3 channels from neuroendocrine cells are stimulated (rather than inhibited) by ligand-bound Gi/Go-coupled GPCRs, an effect mimicked by phorbol ester and blocked by serine/threonine kinase inhibitors but not PI3K inhibitor wortmannin, indicating PKC-dependent regulation distinct from CaV2.2. Xenopus oocyte expression, whole-cell patch-clamp, pharmacological dissection Molecular endocrinology Medium 11435619
2003 Genetic knockout of Cav1.3 in mice abolishes the L-type Ca²⁺ current component activating at diastolic depolarization voltages in sinoatrial node cells, demonstrating that Cav1.3 channels are essential for cardiac pacemaker diastolic depolarization and that their absence causes bradycardia and spontaneous arrhythmia. Gene-targeted knockout mice, patch-clamp recording of sinoatrial node cells, pharmacological L-type current analysis Proceedings of the National Academy of Sciences of the United States of America High 12700358
2003 CaV1.3 channels are the dominant voltage-gated Ca²⁺ channels in cochlear inner hair cells (IHCs); their absence in CaV1.3-/- mice nearly eliminates evoked exocytosis, prevents normal IHC maturation (loss of Ca²⁺ action potentials, failure to acquire BK channels, persistence of efferent cholinergic input), and leaves exocytosis triggered by flash photolysis of caged Ca²⁺ intact, indicating tight coupling of CaV1.3 to exocytosis. Patch-clamp, membrane capacitance measurements, photolysis of caged Ca²⁺, pharmacological channel subtype identification in CaV1.3-/- mice The Journal of neuroscience High 14645476
2005 CaV1.3 channels cluster preferentially at ribbon-type active zones of IHCs (~80 channels/active zone); nonstationary fluctuation analysis estimates ~1700 total channels. Manipulation of single-channel current vs. open-channel number reveals nanodomain Ca²⁺ coupling: RRP exocytosis has high intrinsic Ca²⁺ cooperativity with single-channel current but near-unity apparent cooperativity with channel number, indicating few nearby CaV1.3 channels impose nanodomain [Ca²⁺] on release sites. Nonstationary fluctuation analysis, immunohistochemistry, membrane capacitance recordings, pharmacological manipulation of single-channel current The Journal of neuroscience High 16354915
2005 The long C-terminal splice variant of CaV1.3 (CaV1.3a) contains SH3- and PDZ-binding motifs that directly and specifically associate with the scaffolding protein Shank (yeast two-hybrid, in vitro pull-down); Shank-binding is necessary and sufficient for synaptic clustering of CaV1.3 in hippocampal neurons and is required for CaV1.3-mediated pCREB signaling. Yeast two-hybrid, in vitro binding assay, immunocytochemistry in hippocampal neurons, dominant-negative peptide experiments, dihydropyridine-resistant mutant channels The Journal of neuroscience High 15689539
2005 D2 dopaminergic and M1 muscarinic receptors selectively modulate CaV1.3 (not other L-type channels) in striatal medium spiny neurons; this modulation requires the CaV1.3 PDZ-binding domain and its interaction with Shank, and Shank–Homer interaction, establishing a signaling complex at corticostriatal synapses that enables GPCR regulation of CaV1.3 and glutamatergic integration. Electrophysiology in striatal neurons, intracellular dialysis of competing peptides, CaV1.3 knockout mice, immunocytochemistry The Journal of neuroscience High 15689540
2006 IGF-1/RTK modulates CaV1.3 channels via a PLC→IP3-store Ca²⁺ release→CaMKII cascade; CaMKII phosphorylation of serine S1486 in the EF-hand motif of the CaV1.3 α1 subunit is required, causing a hyperpolarizing shift in current-voltage relationship and potentiation of peak currents, and contributing to pCREB activation. Site-directed mutagenesis (S1486A), pharmacological inhibitors, patch-clamp, pCREB immunostaining in cortical/hippocampal neurons The Journal of neuroscience High 16763033
2006 PKA (via membrane-permeable 8-bromo-cAMP) phosphorylates the CaV1.3 α1 subunit and significantly increases α1D Ca²⁺ channel current density in tsA201 cells; this increase is blocked by the PKA inhibitor PKI, demonstrating PKA-dependent positive modulation of CaV1.3. Heterologous expression in tsA201 cells, whole-cell patch-clamp, pharmacology, Western blot phosphorylation assay American journal of physiology. Heart and circulatory physiology Medium 15615842
2006 PKC inhibits CaV1.3 Ca²⁺ channels through phosphorylation of serine 81 at the N-terminal region; introduction of a phosphomimetic S81D recapitulates inhibition, and dialysis of a competing 35-aa peptide containing S81 prevents PKC modulation; βII- and εPKC isoforms are specifically responsible. Site-directed mutagenesis (S81D), competing peptide dialysis, isoform-specific PKC pharmacology, whole-cell patch-clamp in tsA201 cells American journal of physiology. Heart and circulatory physiology High 16973824
2007 CaBP1, a calmodulin-like Ca²⁺-binding protein, blunts Ca²⁺-dependent inactivation (CDI) of CaV1.3 by interacting with calmodulin-binding sequences in the CaV1.3 α1 subunit; CaBP1 is strongly localized at presynaptic ribbon synapses of adult IHCs and is implicated in conferring anomalously slow CDI required for auditory transmission. CaBP4 interacts with the same sequences but suppresses CDI less efficiently. Co-immunoprecipitation, heterologous expression with patch-clamp, immunolocalization in IHCs, CaBP4-/- mice The Journal of physiology High 17947313
2007 CaV1.3 and RyR2 physically interact via the CaV1.3 N-terminus (identified by yeast two-hybrid and confirmed by co-immunoprecipitation) in rat hippocampus; depolarization activating L-type Ca²⁺ channels triggers RyR2-dependent Ca²⁺ release even without extracellular Ca²⁺, and this effect is blocked by siRNA silencing of CaV1.3. Yeast two-hybrid, co-immunoprecipitation, immunocytochemistry, siRNA knockdown, Ca²⁺ imaging in hippocampal neurons The Journal of biological chemistry High 17823125
2008 Alternative splicing in the CaV1.3 C-terminus generates long (CaV1.3₄₂) and short (CaV1.3₄₂A) forms; the long form contains a C-terminal modulatory domain (CTM) whose removal (short form or CaV1.3ΔC116 truncation) shifts activation to more negative voltages and enhances Ca²⁺-dependent inactivation. FRET experiments confirm intramolecular C-terminal protein interaction that modulates calmodulin binding to the IQ domain. Heterologous expression in HEK-293 cells, whole-cell patch-clamp, FRET, truncation/deletion constructs, co-expression of C-terminal peptide The Journal of biological chemistry High 18482979
2008 The otoferlin C2D domain directly binds the CaV1.3 II-III loop in a Ca²⁺-dependent manner; the deafness-causing mutation L1011P in C2D renders this interaction Ca²⁺-insensitive and greatly reduced, while the C2F domain binds syntaxin 1A and SNAP-25, defining otoferlin as a molecular link between the Ca²⁺ channel and the SNARE complex at IHC synapses. Fusion protein pull-down with disease-associated mutants, Ca²⁺-dependent binding assays, Kd measurements The Journal of biological chemistry High 19004828
2009 Whirlin (USH2D protein) specifically interacts with CaV1.3 via PDZ domain binding (confirmed by yeast two-hybrid, GST pull-down, co-immunoprecipitation); CaV1.3 and whirlin co-localize at the connecting cilium and photoreceptor synapse in adult retina, integrating CaV1.3 into the Usher protein network. Yeast two-hybrid, GST pull-down, co-immunoprecipitation, immunofluorescence and immunoelectron microscopy in retina Investigative ophthalmology & visual science High 19959638
2010 CaV1.3 undergoes Ca²⁺-dependent facilitation (CDF) only when densin and CaMKII are co-expressed together; facilitation requires Ca²⁺, CaMKII activation, CaMKII–densin association, and densin binding to the CaV1.3 α1 C-terminal domain. CaV1.3, densin, and CaMKII form a complex in brain and co-localize at dendritic spines. Heterologous expression in HEK293T cells, co-immunoprecipitation from brain, patch-clamp, dominant-negative CaMKII The Journal of neuroscience High 20392935
2010 CaV1.3 directly associates with GABABR2 via yeast two-hybrid, GST pull-down, and co-immunoprecipitation; GABAB receptor activation increases CaV1.3 (but not CaV1.2) currents and intracellular Ca²⁺, demonstrating subtype-specific functional coupling between GABABR and CaV1.3. Yeast two-hybrid, GST pull-down, co-immunoprecipitation, patch-clamp, Ca²⁺ imaging in HEK293 and hippocampal neurons FEBS letters Medium 20627102
2010 RIM2α binds to the β-subunit of the CaV1.3 channel complex, co-localizes with CaV1.3 at IHC presynaptic active zones, and slows both Ca²⁺-dependent and voltage-dependent inactivation of CaV1.3 channels, generating a non-inactivating current component characteristic of IHC CaV1.3 currents. Co-localization in IHCs, heterologous expression in tsA-201 cells, patch-clamp Molecular and cellular neurosciences Medium 20363327
2010 Loss of function of CACNA1D in humans (insertion of glycine causing non-conducting channels with abnormal voltage-dependent gating) causes SANDD syndrome (sinoatrial node dysfunction and deafness), establishing that CaV1.3 is required for human SAN pacemaking and auditory hair cell function. Positional cloning, Sanger sequencing, heterologous expression with patch-clamp of mutant channels Nature neuroscience High 21131953
2011 Harmonin, a PDZ-domain scaffolding protein required for mechanosensory function, associates with CaV1.3 at IHC presynapses and limits CaV1.3 channel surface availability through a ubiquitin-dependent degradation pathway. Co-immunoprecipitation at IHC synapse, ubiquitin pathway assay, immunofluorescence Nature neuroscience High 21822269
2011 The C-terminus of CaV1.3 translocates to the nucleus in atrial myocytes in a Ca²⁺-dependent manner, where it functions as a transcriptional regulator to modulate SK2 channel expression; CaV1.3 null mice show decreased myosin light chain 2 protein, which interacts with SK2 to regulate its membrane localization. Nuclear fractionation, CaV1.3-/- mouse model, Western blot, co-immunoprecipitation The Journal of biological chemistry Medium 25538241
2012 Zebrafish CaV1.3a channels regulate synaptic ribbon size in hair cells: genetic disruption or acute pharmacological block enlarges ribbons, while channel activation reduces ribbon size and intact synapses. Ca²⁺ influx through CaV1.3a is required for synaptic maintenance; effects are not due to loss of neurotransmission. In vivo Ca²⁺ imaging, confocal and super-resolution microscopy, genetic mutants, pharmacological manipulation, vglut3 mutant controls in zebrafish The Journal of neuroscience High 23197719
2012 CaV1.3 channels in the sinoatrial node co-localize with ryanodine receptors in sarcomeric structures (while CaV1.2 is restricted to delimiting membrane); CaV1.3 undergoes stronger voltage-dependent facilitation (VDF) than CaV1.2 during recovery from inactivation, which enhances pacemaker recovery after pauses via preferential coupling to RyR-mediated Ca²⁺ release. Patch-clamp with DHP-insensitive CaV1.2 knock-in mice to isolate channel-specific currents, immunofluorescence co-localization, computational modeling The Journal of physiology High 23045342
2013 Somatic mutations altering Gly403 or Ile770 in the S6 pore-lining segments of CACNA1D cause gain-of-function in aldosterone-producing adenomas: Gly403 mutations shift activation to less depolarized potentials and impair inactivation; both lead to increased Ca²⁺ influx driving aldosterone production. Identical positions mutated as germline de novo cause primary aldosteronism with neuromuscular abnormalities. Whole-exome sequencing, heterologous expression of mutant channels, whole-cell patch-clamp in tsA-201 cells Nature genetics High 23913001
2013 RNA editing by ADAR2 at the IQ domain of CaV1.3 (within exon 41) reduces Ca²⁺-dependent inactivation (CDI) by weakening prebinding of Ca²⁺-free calmodulin (apoCaM) to the channel rather than attenuating Ca²⁺/CaM binding; this makes CDI continuously tunable by fluctuations in ambient calmodulin levels, an effect confirmed in substantia nigral neurons. Heterologous expression with RNA-edited channels, patch-clamp, calmodulin titration, recordings from substantia nigra neurons Cell reports High 24120865
2013 Harmonin binding to the CaV1.3 α1 distal C-terminus (dCT) enhances voltage-dependent facilitation (VDF) of CaV1.3 currents in HEK293T cells and in mouse IHCs; dfcr harmonin mutant that cannot bind α1 dCT fails to promote VDF and reduces synchronous exocytosis in mature IHCs, demonstrating a multifaceted presynaptic role of harmonin in regulating CaV1.3 and exocytosis. Heterologous expression with mutant harmonin variants, patch-clamp, membrane capacitance recordings in IHCs from dfcr mice The Journal of physiology High 23613530
2014 De novo CACNA1D mutations p.A749G and p.G407R in autism spectrum disorder patients cause gain-of-function: p.A749G shifts voltage-dependence of activation and inactivation ~15 mV negative; p.G407R markedly slows current inactivation; both increase Ca²⁺ influx through CaV1.3. Whole-cell patch-clamp of mutant channels expressed in tsA-201 cells Biological psychiatry High 25620733
2014 The C-terminal modulatory domain (CTM) controls coupling of voltage-sensor movement to pore opening in CaV1.3: the CTM weakens this coupling so that a greater fraction of charge must move before channel opening; removal of CTM (short splice variant CaV1.3₄₂A) enhances coupling efficiency, shifting activation ~7.2 mV negative without affecting voltage-sensor charge movement. Gating current measurement (QON-V) and ionic current recording in tsA-201 cells expressing long and short CaV1.3 splice variants Biophysical journal High 24703308
2015 RIM2α and RIM2β are expressed at IHC active zones and promote clustering of CaV1.3 channels; RIM2α-deficient IHCs have fewer synaptic CaV1.3 channels (confirmed by superresolution microscopy), reduced Ca²⁺ influx, and proportionally reduced exocytosis; RIM2 binds the channel β-subunit. Immunofluorescence, superresolution microscopy, patch-clamp fluctuation analysis, Ca²⁺ imaging, electron tomography, hair cell-specific conditional KO Proceedings of the National Academy of Sciences of the United States of America High 26034270
2015 In substantia nigra dopamine neurons, Cav1.3 L-type Ca²⁺ channel activity, together with internal Ca²⁺ and the neuronal calcium sensor NCS-1, is required for sensitization of D2-autoreceptor responses; Cav1.3 activity promotes NCS-1 interaction with D2 receptors, modulating inhibitory GIRK2-mediated feedback. This pathway is also active in human SN DA neurons and is altered in Parkinson's disease. Electrophysiology in brain slices from Cav1.3 KO and WT mice, pharmacological tools, in vivo manipulation with l-DOPA/cocaine, mRNA analysis of human SN neurons Brain : a journal of neurology High 24934288
2015 The cell-type-specific function of the CaV1.3 C-terminal modulatory domain (CTM) differs between IHCs and chromaffin cells: CTM disruption impairs Ca²⁺-dependent inactivation in IHCs but increases it in chromaffin cells, causing hyperpolarized resting potential and reduced pacemaking in chromaffin cells. Knock-in mice with HA tag disrupting CTM, patch-clamp in IHCs and chromaffin cells, hearing threshold measurement Frontiers in cellular neuroscience High 26379493
2016 Cav1.3 channels provide Ca²⁺ influx during diastolic depolarization in SAN cells that triggers local RyR-dependent Ca²⁺ release events; Cav1.3-/- SAN cells show reduced frequency and impaired synchronization of local Ca²⁺ release, preventing Ca²⁺ transient generation and spontaneous activity. Caffeine-stimulated Ca²⁺-induced Ca²⁺ release rescues pacemaking in Cav1.3-/- cells. Ca²⁺ imaging in isolated SAN cells and ex vivo preparations from Cav1.3-/- and WT mice, action potential voltage-clamp commands, caffeine rescue experiments Cardiovascular research High 26786159
2016 The α2δ2 auxiliary subunit co-assembles with CaV1.3 at IHC presynapses; ducky (α2δ2-null) mice show 30-40% reduction of CaV1.3 Ca²⁺ and Ba²⁺ currents with altered gating, reduced exocytosis proportional to reduced Ca²⁺ influx, and impaired trans-synaptic alignment between presynaptic CaV1.3 clusters and postsynaptic AMPA receptor/PSD-95 clusters. Patch-clamp, immunofluorescence, Ca²⁺ imaging in ducky null mouse IHCs The Journal of neuroscience High 27798183
2017 De novo CACNA1D mutation V401L (in the activation gate) causes gain-of-function in a patient with ASD and epilepsy: significantly increases current density, shifts activation and inactivation to more negative voltages, and reduces inactivation in both long and short CaV1.3 splice variants; mutant channels retain full sensitivity to isradipine. Whole-cell patch-clamp of V401L mutant channels expressed in tsA-201 cells, both splice variants tested Human molecular genetics High 28472301
2018 Brain-selective RNA editing of CaV1.3 transcripts is restricted to neurons by splicing factor SRSF9, which inhibits ADAR2-mediated editing. Mechanistically, SRSF9 directly binds the RNA duplex required for editing (formed between exon 41 and an intronic editing-site complementary sequence), and selective down-regulation of SRSF9 in neurons enables neuron-specific CaV1.3 editing. Minigene editing assay with ADAR2 and SRSF9, CLIP/RIP to demonstrate direct RNA binding, SRSF9 knockdown/overexpression Nucleic acids research High 29733375
2016 An autism-associated de novo mutation A760G (equivalent to A749G in another numbering) severely diminishes Ca²⁺-dependent inactivation (CDI) of CaV1.3 by enhancing channel opening within the Ca²⁺-inactivated mode; simultaneously, A760G increases voltage-dependent inactivation (VDI), creating opposing regulatory effects that together increase intracellular Ca²⁺. Whole-cell patch-clamp of mutant channels, allosteric gating model analysis Scientific reports High 27255217
2020 CACNA1D gain-of-function mutation S652L shifts voltage-dependence of activation and steady-state inactivation ~13-17 mV negative, increases window currents at subthreshold voltages, slows tail currents, and increases Ca²⁺ during AP-like stimuli; it also increases sensitivity to isradipine 3-4-fold. The contrasting loss-of-function S652W mutation shifts gating positive, confirming that only gain-of-function variants confer high disease risk. Whole-cell patch-clamp of mutant and wild-type CaV1.3 in tsA-201 cells, isradipine dose-response Molecular autism High 31921405

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2013 Somatic and germline CACNA1D calcium channel mutations in aldosterone-producing adenomas and primary aldosteronism. Nature genetics 471 23913001
2001 alpha 1D (Cav1.3) subunits can form l-type Ca2+ channels activating at negative voltages. The Journal of biological chemistry 370 11285265
2003 Functional role of L-type Cav1.3 Ca2+ channels in cardiac pacemaker activity. Proceedings of the National Academy of Sciences of the United States of America 367 12700358
2003 CaV1.3 channels are essential for development and presynaptic activity of cochlear inner hair cells. The Journal of neuroscience : the official journal of the Society for Neuroscience 308 14645476
2005 Few CaV1.3 channels regulate the exocytosis of a synaptic vesicle at the hair cell ribbon synapse. The Journal of neuroscience : the official journal of the Society for Neuroscience 237 16354915
2010 Loss of Ca(v)1.3 (CACNA1D) function in a human channelopathy with bradycardia and congenital deafness. Nature neuroscience 234 21131953
2005 G-protein-coupled receptor modulation of striatal CaV1.3 L-type Ca2+ channels is dependent on a Shank-binding domain. The Journal of neuroscience : the official journal of the Society for Neuroscience 216 15689540
2014 CACNA1D de novo mutations in autism spectrum disorders activate Cav1.3 L-type calcium channels. Biological psychiatry 145 25620733
2012 CaV1.3-selective L-type calcium channel antagonists as potential new therapeutics for Parkinson's disease. Nature communications 139 23093183
2005 Association of CaV1.3 L-type calcium channels with Shank. The Journal of neuroscience : the official journal of the Society for Neuroscience 123 15689539
2014 The role of L-type voltage-gated calcium channels Cav1.2 and Cav1.3 in normal and pathological brain function. Cell and tissue research 121 24996399
2008 Modulation of voltage- and Ca2+-dependent gating of CaV1.3 L-type calcium channels by alternative splicing of a C-terminal regulatory domain. The Journal of biological chemistry 119 18482979
2005 Functional roles of Cav1.3(alpha1D) calcium channels in atria: insights gained from gene-targeted null mutant mice. Circulation 115 16172271
2003 Age-related working memory impairment is correlated with increases in the L-type calcium channel protein alpha1D (Cav1.3) in area CA1 of the hippocampus and both are ameliorated by chronic nimodipine treatment. Brain research. Molecular brain research 113 12591156
2003 Cav1.3 (alpha1D) Ca2+ currents in neonatal outer hair cells of mice. The Journal of physiology 111 14514878
2014 Cav1.3 channels control D2-autoreceptor responses via NCS-1 in substantia nigra dopamine neurons. Brain : a journal of neurology 100 24934288
2009 Elementary properties of CaV1.3 Ca(2+) channels expressed in mouse cochlear inner hair cells. The Journal of physiology 97 19917569
2007 Ca2+-binding proteins tune Ca2+-feedback to Cav1.3 channels in mouse auditory hair cells. The Journal of physiology 96 17947313
2017 New gain-of-function mutation shows CACNA1D as recurrently mutated gene in autism spectrum disorders and epilepsy. Human molecular genetics 92 28472301
2012 Presynaptic CaV1.3 channels regulate synaptic ribbon size and are required for synaptic maintenance in sensory hair cells. The Journal of neuroscience : the official journal of the Society for Neuroscience 91 23197719
2008 Direct interaction of otoferlin with syntaxin 1A, SNAP-25, and the L-type voltage-gated calcium channel Cav1.3. The Journal of biological chemistry 89 19004828
2006 Ca1.2 and CaV1.3 neuronal L-type calcium channels: differential targeting and signaling to pCREB. The European journal of neuroscience 86 16706838
2006 The L-Type voltage-gated calcium channel Cav1.3 mediates consolidation, but not extinction, of contextually conditioned fear in mice. Learning & memory (Cold Spring Harbor, N.Y.) 80 17015855
2016 L-type Cav1.3 channels regulate ryanodine receptor-dependent Ca2+ release during sino-atrial node pacemaker activity. Cardiovascular research 79 26786159
2001 Functional properties of Cav1.3 (alpha1D) L-type Ca2+ channel splice variants expressed by rat brain and neuroendocrine GH3 cells. The Journal of biological chemistry 77 11514547
2011 Functional characterization of alternative splicing in the C terminus of L-type CaV1.3 channels. The Journal of biological chemistry 76 21998309
2007 Functional interaction of neuronal Cav1.3 L-type calcium channel with ryanodine receptor type 2 in the rat hippocampus. The Journal of biological chemistry 74 17823125
2010 Ca2+-dependent facilitation of Cav1.3 Ca2+ channels by densin and Ca2+/calmodulin-dependent protein kinase II. The Journal of neuroscience : the official journal of the Society for Neuroscience 72 20392935
2017 A CACNA1D mutation in a patient with persistent hyperinsulinaemic hypoglycaemia, heart defects, and severe hypotonia. Pediatric diabetes 69 28318089
2016 Cav 1.3 (CACNA1D) L-type Ca2+ channel dysfunction in CNS disorders. The Journal of physiology 68 26842699
2012 The human L-type calcium channel Cav1.3 regulates insulin release and polymorphisms in CACNA1D associate with type 2 diabetes. Diabetologia 68 23229155
2011 Harmonin inhibits presynaptic Cav1.3 Ca²⁺ channels in mouse inner hair cells. Nature neuroscience 68 21822269
2001 Functional expression and characterization of a voltage-gated CaV1.3 (alpha1D) calcium channel subunit from an insulin-secreting cell line. Molecular endocrinology (Baltimore, Md.) 68 11435619
1995 Molecular diversity and functional characterization of voltage-dependent calcium channels (CACN4) expressed in pancreatic beta-cells. Molecular endocrinology (Baltimore, Md.) 65 7760845
2015 Clinical and Steroidogenic Characteristics of Aldosterone-Producing Adenomas With ATPase or CACNA1D Gene Mutations. The Journal of clinical endocrinology and metabolism 64 26606680
2005 Novel molecular mechanism involving alpha1D (Cav1.3) L-type calcium channel in autoimmune-associated sinus bradycardia. Circulation 63 15939813
2003 Neurological phenotype and synaptic function in mice lacking the CaV1.3 alpha subunit of neuronal L-type voltage-dependent Ca2+ channels. Neuroscience 63 12890513
2007 Apical GLUT2 and Cav1.3: regulation of rat intestinal glucose and calcium absorption. The Journal of physiology 62 17272350
2013 Cav1.3 channel α1D protein is overexpressed and modulates androgen receptor transactivation in prostate cancers. Urologic oncology 61 24054868
2006 Insulin-like growth factor-1 modulation of CaV1.3 calcium channels depends on Ca2+ release from IP3-sensitive stores and calcium/calmodulin kinase II phosphorylation of the alpha1 subunit EF hand. The Journal of neuroscience : the official journal of the Society for Neuroscience 60 16763033
2006 Synaptic organization in cochlear inner hair cells deficient for the CaV1.3 (alpha1D) subunit of L-type Ca2+ channels. Neuroscience 59 16828974
2008 Biophysical properties of CaV1.3 calcium channels in gerbil inner hair cells. The Journal of physiology 57 18174213
2016 α2δ2 Controls the Function and Trans-Synaptic Coupling of Cav1.3 Channels in Mouse Inner Hair Cells and Is Essential for Normal Hearing. The Journal of neuroscience : the official journal of the Society for Neuroscience 56 27798183
2020 De novo CACNA1D Ca2+ channelopathies: clinical phenotypes and molecular mechanism. Pflugers Archiv : European journal of physiology 55 32583268
2003 Enhanced expression of L-type Cav1.3 calcium channels in murine embryonic hearts from Cav1.2-deficient mice. The Journal of biological chemistry 55 12900400
2015 Rab3-interacting molecules 2α and 2β promote the abundance of voltage-gated CaV1.3 Ca2+ channels at hair cell active zones. Proceedings of the National Academy of Sciences of the United States of America 54 26034270
2015 The L-type calcium channel Cav1.3 is required for proper hippocampal neurogenesis and cognitive functions. Cell calcium 54 26459417
2012 Distinct localization and modulation of Cav1.2 and Cav1.3 L-type Ca2+ channels in mouse sinoatrial node. The Journal of physiology 52 23045342
2011 CaV1.3 channels and intracellular calcium mediate osmotic stress-induced N-terminal c-Jun kinase activation and disruption of tight junctions in Caco-2 CELL MONOLAYERS. The Journal of biological chemistry 51 21737448
2007 Voltage-dependent calcium channel CaV1.3 subunits regulate the light peak of the electroretinogram. Journal of neurophysiology 49 17376851
2014 Regulation of gene transcription by voltage-gated L-type calcium channel, Cav1.3. The Journal of biological chemistry 48 25538241
2013 Continuously tunable Ca(2+) regulation of RNA-edited CaV1.3 channels. Cell reports 48 24120865
2022 tRF-Val-CAC-016 modulates the transduction of CACNA1d-mediated MAPK signaling pathways to suppress the proliferation of gastric carcinoma. Cell communication and signaling : CCS 47 35590368
2009 Association of whirlin with Cav1.3 (alpha1D) channels in photoreceptors, defining a novel member of the usher protein network. Investigative ophthalmology & visual science 47 19959638
2007 Calcium absorption by Cav1.3 induces terminal web myosin II phosphorylation and apical GLUT2 insertion in rat intestine. The Journal of physiology 46 17272349
2004 Localization and modulation of {alpha}1D (Cav1.3) L-type Ca channel by protein kinase A. American journal of physiology. Heart and circulatory physiology 46 15615842
2016 Cav1.2 and Cav1.3 L-type calcium channels independently control short- and long-term sensitization to pain. The Journal of physiology 45 27231046
2010 Modulation of Cav1.3 Ca2+ channel gating by Rab3 interacting molecule. Molecular and cellular neurosciences 43 20363327
2020 Biophysical classification of a CACNA1D de novo mutation as a high-risk mutation for a severe neurodevelopmental disorder. Molecular autism 42 31921405
2015 Cell-type-specific tuning of Cav1.3 Ca(2+)-channels by a C-terminal automodulatory domain. Frontiers in cellular neuroscience 42 26379493
1995 The structures of the human calcium channel alpha 1 subunit (CACNL1A2) and beta subunit (CACNLB3) genes. Genomics 42 7557998
2013 Burst activity and ultrafast activation kinetics of CaV1.3 Ca²⁺ channels support presynaptic activity in adult gerbil hair cell ribbon synapses. The Journal of physiology 41 23713031
2017 Aldosterone-Producing Adenomas: Histopathology-Genotype Correlation and Identification of a Novel CACNA1D Mutation. Hypertension (Dallas, Tex. : 1979) 40 28584016
2015 Evaluation of genetic susceptibility of common variants in CACNA1D with schizophrenia in Han Chinese. Scientific reports 40 26255836
2004 Disturbed atrio-ventricular conduction and normal contractile function in isolated hearts from Cav1.3-knockout mice. Naunyn-Schmiedeberg's archives of pharmacology 40 15146309
2015 Cav1.3 Channels as Key Regulators of Neuron-Like Firings and Catecholamine Release in Chromaffin Cells. Current molecular pharmacology 38 25966692
2012 Retrocochlear function of the peripheral deafness gene Cacna1d. Human molecular genetics 38 22678062
1991 A brain L-type calcium channel alpha 1 subunit gene (CCHL1A2) maps to mouse chromosome 14 and human chromosome 3. Genomics 38 1664412
2018 Identification of CACNA1D variants associated with sinoatrial node dysfunction and deafness in additional Pakistani families reveals a clinical significance. Journal of human genetics 37 30498240
2015 Compensatory T-type Ca2+ channel activity alters D2-autoreceptor responses of Substantia nigra dopamine neurons from Cav1.3 L-type Ca2+ channel KO mice. Scientific reports 36 26381090
2014 CaV1.3 L-type channels, maxiK Ca(2+)-dependent K(+) channels and bestrophin-1 regulate rhythmic photoreceptor outer segment phagocytosis by retinal pigment epithelial cells. Cellular signalling 35 24407175
2010 Expression and roles of Cav1.3 (α1D) L-type Ca²+ channel in atrioventricular node automaticity. Journal of molecular and cellular cardiology 35 20951705
2017 Ca2+ protein alpha 1D of CaV1.3 regulates intracellular calcium concentration and migration of colon cancer cells through a non-canonical activity. Scientific reports 34 29079724
2016 Regulation of aldosterone secretion by Cav1.3. Scientific reports 32 27098837
2012 Equal sensitivity of Cav1.2 and Cav1.3 channels to the opposing modulations of PKA and PKG in mouse chromaffin cells. The Journal of physiology 32 22826131
2008 CaV1.2 rather than CaV1.3 is coupled to glucose-stimulated insulin secretion in INS-1 832/13 cells. Journal of molecular endocrinology 32 18562674
2020 A de novo CACNA1D missense mutation in a patient with congenital hyperinsulinism, primary hyperaldosteronism and hypotonia. Channels (Austin, Tex.) 31 32336187
2014 C-terminal modulatory domain controls coupling of voltage-sensing to pore opening in Cav1.3 L-type Ca(2+) channels. Biophysical journal 31 24703308
2013 Harmonin enhances voltage-dependent facilitation of Cav1.3 channels and synchronous exocytosis in mouse inner hair cells. The Journal of physiology 31 23613530
2012 Cav1.3 and Cav1.2 channels of adrenal chromaffin cells: emerging views on cAMP/cGMP-mediated phosphorylation and role in pacemaking. Biochimica et biophysica acta 31 23159773
2008 Expression of calcium channel CaV1.3 in cat spinal cord: light and electron microscopic immunohistochemical study. The Journal of comparative neurology 30 18095323
2016 An autism-associated mutation in CaV1.3 channels has opposing effects on voltage- and Ca(2+)-dependent regulation. Scientific reports 29 27255217
2019 Genetic silencing of striatal CaV1.3 prevents and ameliorates levodopa dyskinesia. Movement disorders : official journal of the Movement Disorder Society 27 31002755
2009 Cav1.2 and Cav1.3 are differentially coupled to glucagon-like peptide-1 potentiation of glucose-stimulated insulin secretion in the pancreatic beta-cell line INS-1. The Journal of pharmacology and experimental therapeutics 27 19710366
2015 LRP1B, BRD2 and CACNA1D: new candidate genes in fetal metabolic programming of newborns exposed to maternal hyperglycemia. Epigenomics 25 26586120
2009 The intracellular II-III loops of Cav1.2 and Cav1.3 uncouple L-type voltage-gated Ca2+ channels from glucagon-like peptide-1 potentiation of insulin secretion in INS-1 cells via displacement from lipid rafts. The Journal of pharmacology and experimental therapeutics 25 19351867
2018 Tissue-selective restriction of RNA editing of CaV1.3 by splicing factor SRSF9. Nucleic acids research 24 29733375
2012 Structural determinants of CaV1.3 L-type calcium channel gating. Channels (Austin, Tex.) 24 22760075
2006 Differential modulation of Cav1.2 and Cav1.3-mediated glucose-stimulated insulin secretion by cAMP in INS-1 cells: distinct roles for exchange protein directly activated by cAMP 2 (Epac2) and protein kinase A. The Journal of pharmacology and experimental therapeutics 23 16565168
2006 Protein kinase C activation inhibits Cav1.3 calcium channel at NH2-terminal serine 81 phosphorylation site. American journal of physiology. Heart and circulatory physiology 23 16973824
2010 Direct interaction and functional coupling between voltage-gated CaV1.3 Ca2+ channel and GABAB receptor subunit 2. FEBS letters 22 20627102
2005 Subtype switching of L-Type Ca 2+ channel from Cav1.3 to Cav1.2 in embryonic murine ventricle. Circulation journal : official journal of the Japanese Circulation Society 22 16247219
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
2018 [The third case report a patient with primary aldosteronism, seizures, and neurologic abnormalities (PASNA) syndrome de novo variant mutations in the CACNA1D gene]. Zhurnal nevrologii i psikhiatrii imeni S.S. Korsakova 21 30698561
2009 Enhancement of calcium transport in Caco-2 monolayer through PKCzeta-dependent Cav1.3-mediated transcellular and rectifying paracellular pathways by prolactin. American journal of physiology. Cell physiology 21 19339512
2016 Rescuing cardiac automaticity in L-type Cav1.3 channelopathies and beyond. The Journal of physiology 20 27374078
2017 Reduction of Cav1.3 channels in dorsal hippocampus impairs the development of dentate gyrus newborn neurons and hippocampal-dependent memory tasks. PloS one 19 28715454
2016 A Rare Variant in CACNA1D Segregates with 7 Bipolar I Disorder Cases in a Large Pedigree. Molecular neuropsychiatry 19 27867939
2004 Cav1.3 is preferentially coupled to glucose-induced [Ca2+]i oscillations in the pancreatic beta cell line INS-1. Molecular pharmacology 19 15102955
2011 Perinatal and postnatal expression of Cav1.3 α1D Ca²⁺ channel in the rat heart. Pediatric research 18 21378599