Voltage-dependent L-type calcium channel subunit alpha-1C · UniProt Q13936
CACNA1C encodes the pore-forming α1C subunit of the Cav1.2 L-type voltage-gated calcium channel, which serves as a Ca2+-entry hub and signaling scaffold that couples membrane depolarization to excitation-contraction coupling, neuronal plasticity, and Ca2+-dependent transcription (PMID:11441182, PMID:16251435, PMID:15132976). Cav1.2 nucleates a macromolecular signaling complex in which a β2-adrenergic receptor, G protein, adenylyl cyclase, PKA and PP2A are physically tethered for local, specific regulation (PMID:11441182); channel gating is tuned by convergent phosphorylation, with PKA and PKC both targeting Ser1928 on the α1C C-terminus (PMID:15509562), PKG phosphorylating α1C and the β2a subunit to inhibit current (PMID:17626895), and CaMKII binding the β2a subunit to drive a high-activity gating mode (PMID:20194790). Two phosphosites partition basal from stimulated activity: Ser1700 maintains basal L-type current and supports β-adrenergic potentiation (PMID:25368181), while PKA phosphorylation of Ser1928 displaces the associated β2AR to render the channel refractory to further adrenergic stimulation (PMID:27103070), a regulation that itself requires the auxiliary β subunit binding site (PMID:30422117). Ca2+/calmodulin and the related CaBP1 compete at the C-terminal IQ region to set Ca2+-dependent inactivation versus facilitation (PMID:12944271, PMID:15140941). Channel abundance and surface delivery are controlled by auxiliary and trafficking proteins including α2δ-1, BIN1, Rab25, the PIKfyve/lysosomal and ERα/Mdm2 ubiquitin–proteasome degradation routes, and by alternative splicing through Fox proteins and transcriptional inputs from NFAT5 and TDP-43 (PMID:19564422, PMID:19841139, PMID:19797702, PMID:22138472, PMID:27368804, PMID:31355778, PMID:31012223, PMID:27076616). Downstream, Cav1.2 Ca2+ influx — and in some contexts a Ca2+-flux-independent, β2-subunit/H-Ras-dependent route (PMID:30150369) — drives calcineurin/NFAT, CaMKII/HDAC, and Ras/ERK/CREB transcriptional programs governing cardiac hypertrophy, jaw and bone morphogenesis, smooth muscle contraction, hippocampal late-LTP and memory, and neuronal survival (PMID:16251435, PMID:21111744, PMID:23549079, PMID:29202453, PMID:15132976, PMID:27066530). A gain-of-function G406R mutation underlies Timothy syndrome, acting dominantly even in non-excitable cells (PMID:23752588).
Establishing the chromosomal locus of the cardiac dihydropyridine-sensitive Ca2+ channel α1 subunit gave the molecular anchor for all subsequent CACNA1C genetics.
Evidence PCR mapping of human-rodent somatic cell hybrids
It was unknown how β-adrenergic signals reach Cav1.2 with such speed and specificity; identifying a receptor-channel macromolecular complex showed signaling is hardwired by physical proximity.
Evidence Reciprocal Co-IP and electrophysiology in hippocampal neurons identifying β2AR, G protein, adenylyl cyclase, PKA, PP2A on Cav1.2
How Cav1.2 senses its own Ca2+ flux was unclear; mapping apoCaM/Ca2+-CaM binding to the C-terminal IQ/A/C regions defined the molecular basis of Ca2+-dependent inactivation.
Evidence Fluorescence and peptide competition binding assays with IQ-motif mutagenesis
Convergence of kinase inputs was unknown; demonstrating PKC binds the C-terminus and phosphorylates Ser1928 — the same PKA site — revealed an integration node for distinct signaling pathways.
Evidence In vitro kinase assay, Co-IP, site-directed mutagenesis, metabolic labeling in cells
Whether a CaM relative could reverse channel feedback was untested; CaBP1 was shown to compete with CaM at the IQ motif and convert inactivation to facilitation, diversifying Ca2+ feedback.
Evidence Co-IP, PSD fractionation, immunofluorescence, whole-cell electrophysiology
The requirement of Cav1.2 for smooth muscle contraction was inferred but not genetically proven; smooth-muscle KO established it as essential and non-redundant for bladder contractility.
Evidence Smooth muscle-specific conditional KO with electrophysiology and contractility/pharmacology
The role of Cav1.2 in long-term plasticity was unknown; conditional KO showed it is selectively required for protein-synthesis-dependent late-LTP, spatial memory, and CREB-dependent transcription.
Evidence Hippocampus/cortex conditional KO with LTP, behavior, and biochemical signaling assays
How cGMP signaling restrains Cav1.2 was unknown; PKGIα phosphorylation of α1C and β2a Ser496 was shown to inhibit current.
Evidence In vitro kinase assay, phospho-specific antibodies, patch clamp, mutagenesis in HEK and myocytes
How channel electrophysiology is tuned developmentally was unclear; Fox1/Fox2 were shown to direct alternative splicing of exons 9* and 33, generating variants with distinct properties.
Evidence siRNA/overexpression, minigene reporters, RT-PCR in cortical neurons
Activity-dependent removal of Cav1.2 was uncharacterized; NMDAR-driven PIKfyve binding was shown to target the channel to lysosomes, linking degradation to excitotoxicity protection.
Evidence Co-IP, live imaging, siRNA, fractionation, toxicity assays
Determinants of Cav1.2 surface expression in vasculature were unknown; α2δ-1 was shown to be essential for membrane trafficking and myogenic tone.
Evidence Surface biotinylation, shRNA, patch clamp, pressurized myography
An N-terminal modulator of cardiac Cav1.2 was unknown; KChIP2 was shown to bind the N-terminus and modulate I_Ca,L, with compensatory CACNB2 upregulation upon loss.
Evidence Co-IP, patch clamp, gene-chip/PCR in KChIP2 KO mice
Multiple trafficking and gating regulators were defined in cardiac and vascular myocytes: CaMKII/β2a gating-mode control, Rem GTPase gating arrest, Rab25 surface delivery, and ROS/NF-κB transcriptional control of channel abundance.
Evidence Mutagenesis and single-channel/whole-cell electrophysiology in myocytes; immunoFRET; Ca2+/ROS imaging and reporter assays
PMID:20194790 PMID:20616312 PMID:20616314 PMID:27076616
Whether Cav1.2 Ca2+ load drives pathological remodeling was unproven; β2a-mediated influx was shown sufficient to induce hypertrophy via calcineurin/NFAT and CaMKII/HDAC.
Evidence Transgenic and adenoviral β2a overexpression with pathway inhibition and NFAT/HDAC translocation assays
How Cav1.2 reaches cardiac T-tubules and its relevance to heart failure was unknown; BIN1 was identified as the trafficking factor, reduced in failing hearts.
Evidence Human myocyte imaging, T-tubule fractionation, patch clamp, mouse shRNA, zebrafish morpholino
Roles of Cav1.2 in development and non-excitable cells were unclear; influx-driven calcineurin signaling shapes jaw morphogenesis, and the Timothy syndrome G406R mutation acts dominantly via Fstl1/BMP signaling even without measurable currents.
Evidence Mouse gain/loss-of-function, zebrafish, pharmacology; TS-Cav1.2 transgenic with Fstl1 analysis in hair follicle stem cells
An immune role was undefined; Cav1.2 was shown to be selectively expressed in TH2 lymphocytes where PKC-dependent activation controls Ca2+ entry and cytokine output.
Evidence Antisense knockdown, PKC modulation, Ca2+ imaging, cytokine assays in primary human T cells
How basal and β-adrenergic-stimulated cardiac current is set was unresolved; Ser1700 phosphorylation was shown essential for basal I_Ca,L and incremental β-adrenergic potentiation in vivo.
Evidence S1700A knock-in mice, patch clamp, cardiac function and exercise testing
Store-operated coupling to Cav1.2 was unclear; Homer proteins were shown to bridge STIM1 to α1C, with Homer disruption enhancing Cav1.2 Ca2+ entry.
Evidence Co-IP, Homer1 siRNA, dominant-negative peptide, Ca2+ imaging in HEK cells
A developmental survival role in auditory circuits was unknown; embryonic Cav1.2 deletion reduced auditory nuclei volume and cell number and altered LSO firing.
Evidence Conditional KO, brainstem electrophysiology, volumetric/cell-count and ABR analysis
The link between Cav1.2 and transcription/desensitization deepened: PKA-Ser1928 displaces β2AR to limit adrenergic responsiveness, NFAT5 and ROS-driven transcription control channel abundance, and behavioral/affective roles were dissected across brain regions and cell types.
Evidence S1928A knock-in with Co-IP/electrophysiology; NFAT5 promoter binding and zebrafish rescue; region/temporally specific conditional KOs with behavior and plasticity assays
PMID:27066530 PMID:27103070 PMID:27368804 PMID:27922594 PMID:28165117 PMID:28696432
Whether Cav1.2 signals to the nucleus independent of Ca2+ transport was unknown; depolarization was shown to drive Ras/ERK/CREB nuclear signaling via β2-subunit/H-Ras interaction, requiring pore Ca2+ occupancy but not flux.
Evidence Channel mutants (Ca2+-impermeable, CaM-binding, W440A), recombinant H-Ras/β2 pulldowns, reporter assays in cell lines
Auxiliary β subunits, transcriptional control by TDP-43, and ERα/Mdm2-mediated ubiquitination were shown to govern Cav1.2 regulation, expression, and degradation across heart, pancreatic β cells, and neurons.
Evidence β-binding-deficient α1C transgenic and viral pharmacology; β-cell Tardbp KO with Cav1.2 rescue; ubiquitin mutants, Mdm2 overexpression, proteasome inhibition in vivo
PMID:30422117 PMID:31012223 PMID:31355778
How Cav1.2 integrates with Ca2+-release machinery in vascular microdomains was unclear; ANO1-Cav1.2-IP3R were shown to co-assemble to sustain serotonin-induced arterial contraction.
Evidence Co-IP, superresolution microscopy, smooth-muscle ANO1 ablation, pharmacology, GCaMP imaging
The microcircuit role of Cav1.2 in primate cognition was undefined; in dPFC spines it was localized near ER and coupled to SK3, producing an inverted-U dependence of firing on L-type channel activity for working memory.
Evidence EM/light microscopy, pharmacology during unit recording in behaving macaques, transcriptomics
| Year | Finding | Method | Journal | Conf | PMIDs |
|---|---|---|---|---|---|
| 2001 | The β2 adrenergic receptor forms a direct macromolecular signaling complex with Cav1.2, also containing a G protein, adenylyl cyclase, PKA, and PP2A, enabling highly localized and specific signal transduction from receptor to channel in hippocampal neurons. | Co-immunoprecipitation, electrophysiology in hippocampal neurons | Science | High | 11441182 |
| 2004 | PKC isoforms form a macromolecular complex with the α1c subunit of Cav1.2 via direct interaction with the C-terminus, and phosphorylate Ser1928 both in vitro and in vivo, the same residue phosphorylated by PKA, indicating convergence of PKA and PKC signaling on Cav1.2 at Ser1928. | In vitro kinase assay, Co-immunoprecipitation, site-directed mutagenesis, metabolic labeling in intact cells | The Journal of biological chemistry | High | 15509562 |
| 2003 | Apocalmodulin (apoCaM) binds with higher affinity to the C-IQ region of Cav1.2 than to the IQ peptide alone; Ca2+-CaM binds all three C-terminal regions (A, C, IQ); binding to IQ and C peptides increases Ca2+ affinity of the C-lobe of CaM; apoCaM binding to the IQ motif is necessary for rapid Ca2+ binding to the C-lobe and subsequent Ca2+-dependent inactivation. Double mutation of IQ motif residues reduces apoCaM interaction. | Fluorescence binding assays, peptide competition assays, site-directed mutagenesis of IQ motif in channel | Biophysical journal | High | 12944271 |
| 2004 | CaBP1 (Ca2+-binding protein-1) directly interacts with the α1 subunit of Cav1.2 at IQ domain and other CaM-binding sites; IQ binding is Ca2+-dependent and competitive with CaM. CaBP1 co-purifies with Cav1.2 in postsynaptic density fractions from rat brain and colocalizes in neuronal dendrites. CaBP1 prevents Ca2+-dependent inactivation and causes Ca2+-dependent facilitation of Cav1.2 currents, contrasting with CaM's promotion of inactivation. | Co-immunoprecipitation, postsynaptic density fractionation, double-label immunofluorescence, whole-cell electrophysiology in transfected cells | The Journal of neuroscience | High | 15140941 |
| 2005 | Conditional knockout of Cav1.2 (CACNA1C) in hippocampus and neocortex selectively abolishes protein synthesis-dependent, NMDAR-independent late-phase LTP (L-LTP) at Schaffer collateral/CA1 synapses, impairs hippocampus-dependent spatial memory, and decreases MAPK pathway activation and CRE-dependent transcription in CA1 pyramidal neurons. | Conditional knockout mouse (Cav1.2 HCKO), electrophysiology (LTP recording), spatial memory behavioral assays, biochemical signaling assays | The Journal of neuroscience | High | 16251435 |
| 2007 | Protein kinase G (PKGIα) phosphorylates specific residues within both the α1c and β2a subunits of Cav1.2 in vitro and in intact HEK cells and cardiac myocytes; PKG-mediated inhibition of Cav1.2 whole-cell current is significantly reduced by alanine substitution of Ser496 on the β2a subunit. | In vitro kinase assay, phospho-epitope-specific antibodies, whole-cell patch clamp, site-directed mutagenesis | Circulation research | High | 17626895 |
| 2009 | Fox family splicing regulators (Fox1 and Fox2) directly control alternative splicing of CaV1.2 exons 9* and 33 during cortical development: Fox proteins repress exon 9* inclusion and enhance exon 33 inclusion via binding elements in adjacent introns, generating splice variants with distinct electrophysiological properties. | siRNA knockdown, overexpression of Fox1/Fox2, minigene reporter assays, RT-PCR of endogenous CaV1.2 mRNA in cortical neurons | Molecular and cellular biology | High | 19564422 |
| 2009 | NMDA receptor activation causes internalization and lysosomal degradation of CaV1.2 channels through binding to PIKfyve (phosphatidylinositol 3-phosphate 5-kinase), which generates PtdIns(3,5)P2 and promotes CaV1.2 targeting to lysosomes; PIKfyve knockdown prevents CaV1.2 degradation and increases neuronal susceptibility to excitotoxicity. | Immunoprecipitation, live imaging, siRNA knockdown, biochemical fractionation, toxicity assays | The Journal of cell biology | High | 19841139 |
| 2009 | α2δ-1 is the sole α2δ isoform in cerebral artery myocytes, is essential for plasma membrane expression of Cav1.2 α1 subunits, and directly regulates CaV1.2 current; α2δ-1 knockdown reduces surface Cav1.2, decreases intracellular Ca2+ concentration, and inhibits pressure-induced vasoconstriction (myogenic tone). | Surface biotinylation, shRNA knockdown, patch-clamp electrophysiology, pressurized vessel myography, confocal microscopy | Circulation research | High | 19797702 |
| 2010 | CaMKII binding to β2a subunit residue Leu493 and phosphorylation of Thr498 are required for CaV1.2 to enter a high-activity gating mode (mode 2); expression of T498A or L493A β2a mutants reduces Ca2+ entry through Cav1.2, inhibits early afterdepolarizations (EADs), and improves cardiomyocyte survival in CaMKII-overloaded conditions. | Site-directed mutagenesis, patch-clamp electrophysiology (single-channel and whole-cell), adenoviral overexpression in adult rabbit ventricular myocytes, cell survival assays | Proceedings of the National Academy of Sciences of the United States of America | High | 20194790 |
| 2010 | Rem GTPase inhibits Cav1.2 in heart primarily by arresting surface channels in a low open-probability gating mode (not by reducing channel trafficking); this inhibition requires GTP-binding but not membrane targeting, and Rem-inhibited channels cannot be rescued by PKA-dependent phosphorylation but can be rescued by Bay K 8644. | Patch-clamp electrophysiology (whole-cell and gating charge measurements), overexpression in adult guinea pig cardiomyocytes, dominant-negative and chimeric Rem mutants | Circulation research | High | 20616312 |
| 2010 | Increasing L-type Ca2+ influx through Cav1.2 (via β2a subunit overexpression) is sufficient to induce pathological cardiomyocyte hypertrophy through calcineurin/NFAT and CaMKII/HDAC signaling pathways; both cytosolic and SR/ER-nuclear envelope Ca2+ pools are involved. | Transgenic mouse models with β2a overexpression, adenoviral overexpression in cultured cardiomyocytes, L-type channel blockade, calcineurin/CaMKII inhibition, NFAT/HDAC translocation assays | Journal of molecular and cellular cardiology | High | 21111744 |
| 2010 | IP3R-mediated SR Ca2+ release elevates mitochondrial [Ca2+], induces mitochondrial ROS generation, which activates NF-κB to stimulate CaV1.2 channel transcription in arterial myocytes, thereby modulating vasoconstriction. | Mitochondrial Ca2+ imaging, ROS measurements, NF-κB reporter assays, siRNA knockdown, qRT-PCR, patch-clamp, pressurized myography | Circulation research | Medium | 20616314 |
| 2011 | BIN1 (bridging integrator 1) traffics Cav1.2 to cardiac T-tubules; BIN1 is significantly reduced in failing human cardiomyocytes, and this reduction impairs Cav1.2 trafficking to T-tubules, reduces surface Ca2+ current, and impairs calcium transients and contractility. | Confocal imaging of human failing/non-failing myocytes, T-tubule biochemical fractionation, patch clamp, shRNA knockdown in mouse cardiomyocytes, zebrafish morpholino knockdown | Heart rhythm | High | 22138472 |
| 2013 | Ca2+ influx through CaV1.2 regulates jaw/mandible development by controlling cellular hypertrophy and hyperplasia via the calcineurin signaling pathway in jaw primordium cells; CaV1.2 is expressed in first and second pharyngeal arch cells. | Gain-of-function and loss-of-function mouse models, zebrafish knockdown/rescue, pharmacological blockade, calcineurin pathway assays | The Journal of clinical investigation | High | 23549079 |
| 2013 | Timothy syndrome (TS) gain-of-function mutation G406R in Cav1.2 acts in a dominant-negative manner in hair follicle stem cells to delay anagen; Cav1.2 regulates production of the BMP inhibitor follistatin-like1 (Fstl1) from the bulge to derepress stem cell quiescence. This occurs in the absence of detectable voltage-dependent Ca2+ currents in these non-excitable cells. | Transgenic mouse expressing TS-Cav1.2, L-type channel blocker treatment, Fstl1 expression analysis, hair follicle stem cell assays | Genes & development | Medium | 23752588 |
| 2014 | Phosphorylation of Ser1700 on Cav1.2 is essential for maintaining basal L-type Ca2+ current in cardiomyocytes and for the incremental increase by β-adrenergic receptor stimulation (isoproterenol); Ser1700Ala knock-in mice develop cardiac hypertrophy and have reduced stress-induced exercise tolerance. | Knock-in mouse model (S1700A), patch-clamp electrophysiology in neonatal and adult cardiomyocytes, in vivo cardiac function assays, exercise testing | Proceedings of the National Academy of Sciences of the United States of America | High | 25368181 |
| 2016 | Phosphorylation of Cav1.2 Ser1928 by PKA, within the β2AR binding site (residues 1923-1942), displaces the β2AR from Cav1.2 upon β-adrenergic stimulation, rendering Cav1.2 refractory to further β-adrenergic stimulation for several minutes; this effect is lost in S1928A knock-in mice. Long-term potentiation induced by prolonged theta tetanus requires Cav1.2 and its regulation by channel-associated β2AR. | S1928A knock-in mice, Co-immunoprecipitation, electrophysiology (patch clamp and LTP recording), β-adrenergic stimulation assays | The EMBO journal | High | 27103070 |
| 2016 | Deletion of cacna1c in the adult mouse prefrontal cortex produces antidepressant-like effects and reduces REDD1 protein levels; REDD1 overexpression in the PFC of cacna1c heterozygous mice reverses the antidepressant-like phenotype and is associated with lower phospho-Akt (S473) and higher nuclear FoxO3a levels. | Viral vector-mediated conditional knockout, behavioral assays (SPT, FST, TST), molecular signaling assays (REDD1, Akt, FoxO3a) | Neuropsychopharmacology | Medium | 27922594 |
| 2016 | NFAT5 binds to a consensus sequence (TGGAAGCGTTC) in the promoter of Cacna1c and activates its transcription; siRNA-mediated NFAT5 knockdown suppresses Cacna1c expression and decreases L-type Ca2+ current in mouse neonatal cardiomyocytes; morpholino knockdown of nfat5 in zebrafish prevents cacna1c expression and results in non-contractile ventricle, rescued by overexpression of either cacna1c or nfat5. | Promoter analysis, ChIP/binding assay, siRNA knockdown, patch clamp, zebrafish morpholino knockdown with rescue | Journal of molecular medicine | High | 27368804 |
| 2017 | Increased Ca2+ influx through CaV1.2 in osteoblasts activates osteogenic transcriptional programs, promotes mineralization, and inhibits osteoclast activity through increased osteoprotegerin secretion; CaV1.2 is expressed in proliferating chondrocytes and osteoblasts in developing bone. | Transgenic gain-of-function CaV1.2 mutant mice (Prx1-, Col2a1-, Col1a1-Cre), BMSC primary cultures, osteoprotegerin assays, ovariectomy bone-loss model | JCI insight | Medium | 29202453 |
| 2018 | Membrane depolarization triggers nuclear signaling (c-Fos and MeCP2 activation via Ras/ERK/CREB pathway) through Cav1.2 in a Ca2+-influx-independent manner; this requires the intracellular β2 subunit's interaction with H-Ras and is dependent on Ca2+ occupancy of the open channel pore but not Ca2+ transport. Loss of α1-β2 interaction (W440A mutation) or absence of β2 abolishes nuclear signaling. | Mutagenesis (Ca2+-impermeable channel α1L745P, CaM-binding disrupting α1I1624A, α1W440A), pulldown assays with recombinant H-Ras and β2, transfection in HEK293 and SH-SY5Y cells, reporter assays for c-Fos/MeCP2 | Proceedings of the National Academy of Sciences of the United States of America | High | 30150369 |
| 2019 | CaV1.2 β subunits are dispensable for channel trafficking to the sarcolemma in adult cardiomyocytes but are required for β-adrenergic regulation of Cav1.2 and positive inotropy; transgenic α1C lacking the β-subunit binding site traffics normally but cannot be stimulated by isoproterenol. | Transgenic mouse expressing β-binding-deficient α1C, patch clamp, contractility assays in isolated cardiomyocytes and intact heart, viral β-subunit-sequestering peptide | The Journal of clinical investigation | High | 30422117 |
| 2019 | TDP-43 regulates CaV1.2 expression in pancreatic β cells; TDP-43 loss (nuclear depletion) downregulates CaV1.2 and inhibits exocytosis, reducing early-phase insulin secretion; overexpression of CaV1.2 restores early-phase insulin secretion in Tardbp-knockdown MIN6 cells. | β cell-specific Tardbp knockout mice, MIN6 cell siRNA knockdown, CaV1.2 overexpression rescue, insulin secretion assays, exocytosis measurements | The Journal of clinical investigation | High | 31355778 |
| 2019 | Estrogen receptor α (ERα) promotes Cav1.2 ubiquitination and proteasomal degradation in neurons via K29-linked ubiquitin chains and the E3 ligase Mdm2, utilizing the PEST sequence in Cav1.2; ERα agonist administration reduces cerebral Cav1.2 protein and increases Cav1.2 ubiquitination in OVX APP/PS1 mice. | Ubiquitin mutant (K29R), TRABID overexpression, Mdm2 overexpression, MG132 proteasome inhibitor, in vivo ERα agonist (PPT) treatment, immunofluorescence colocalization in vivo | Aging cell | Medium | 31012223 |
| 2020 | Ketamine directly inhibits Cav1.2 calcium channels and blocks Cav1.2-mediated induction of immediate early genes and transcription factors in smooth muscle; Cav1.2-specific inactivation in smooth muscle mimics the ketamine cystitis phenotype, and Cav1.2 agonist Bay K 8644 reverses ketamine-induced smooth muscle dysfunction. | Patch-clamp electrophysiology, smooth muscle-specific Cav1.2 conditional knockout, pharmacological rescue with Bay K 8644, gene expression assays | Nature communications | High | 32859919 |
| 2015 | Homer proteins mediate the physical interaction between STIM1 and the Cav1.2 α1 subunit; store depletion (thapsigargin) induces co-immunoprecipitation of Homer1 with STIM1 and Cav1.2 α1; disruption of Homer function (PPKKFR peptide or siRNA Homer1) reduces STIM1-Cav1.2 association and enhances nifedipine-sensitive Ca2+ entry through Cav1.2. | Co-immunoprecipitation, siRNA knockdown of Homer1, dominant-negative PPKKFR peptide, Ca2+ imaging in HEK-293 cells expressing Cav1.2 subunits | Biochimica et biophysica acta | Medium | 25712868 |
| 2010 | Rab25 GTPase co-localizes with Cav1.2 in cerebral artery myocytes and is required for surface expression of Cav1.2 channels; Rab25 knockdown reduces both surface and intracellular Cav1.2 abundance through lysosomal and proteasomal degradation, decreases whole-cell CaV1.2 current, and inhibits pressure-induced vasoconstriction. | immunoFRET microscopy, surface biotinylation, siRNA knockdown, patch-clamp electrophysiology, pressurized myography | American journal of physiology. Cell physiology | Medium | 27076616 |
| 2010 | α5β1-integrin engagement by fibronectin acutely enhances Cav1.2 current and forms a macromolecular complex with Cav1.2; co-association requires cell adhesion to fibronectin and Cav1.2 C-terminal residues Ser1901, Tyr2122, and two proline-rich domains; phosphorylation at Y2122 and/or S1901 and c-Src binding to PRDs mediate current potentiation. | Co-immunoprecipitation, site-directed mutagenesis of Cav1.2, patch-clamp electrophysiology, confocal immunofluorescence | American journal of physiology. Cell physiology | Medium | 21178109 |
| 2004 | Smooth muscle-specific knockout of Cav1.2 (SMACKO) abolishes L-type calcium current, protein, and spontaneous contractile activity in the bladder; K+- and carbachol-induced contractions are reduced ~10-fold; Rho-kinase and Ca2+-release pathways cannot compensate for the absence of Cav1.2. CCh-induced contraction requires extracellular Ca2+ but not PLC or intracellular Ca2+ stores. | Smooth muscle-specific conditional knockout mouse, electrophysiology, contractility assays, pharmacological dissection | FASEB journal | High | 15132976 |
| 2009 | KChIP2 directly interacts with the amino-terminus of CaV1.2 (confirmed by co-immunoprecipitation) and functionally modulates the cardiac L-type Ca2+ current; KChIP2 knockout mice show decreased ICa,L and compensatory transcriptional upregulation of the calcium channel β2 subunit (CACNB2). | Co-immunoprecipitation, patch-clamp electrophysiology, gene-chip and real-time PCR in KChIP2(-/-) mice | Channels (Austin, Tex.) | Medium | 19713767 |
| 2013 | PKC-dependent activation of Cav1.2 channels selectively controls human TH2 lymphocyte Ca2+ entry and cytokine responses; Cav1.2 is selectively expressed and maintained in TH2 but not TH1 or TH9 cells; both nicardipine and Cav1.2-specific antisense oligonucleotides decrease Ca2+ and cytokine responses in TH2 cells. | Flow cytometry, antisense oligonucleotide knockdown, PKC inhibition/activation, Ca2+ imaging, cytokine assays in primary human T cells | The Journal of allergy and clinical immunology | Medium | 24365142 |
| 2016 | Forebrain-specific conditional knockout of cacna1c in adult mice improved cognitive flexibility and strengthened synaptic plasticity, while embryonic deletion caused cognitive decline, impaired synaptic plasticity, reduced sociability, hyperactivity, and increased anxiety-like behavior, demonstrating a differential developmental vs adult role for Cav1.2. | Conditional knockout (embryonic vs. adult timing using inducible Cre), synaptic plasticity recordings, behavioral phenotyping, chronic stress exposure | Molecular psychiatry | High | 28696432 |
| 2016 | Cacna1c deletion specifically in nucleus accumbens neurons increases susceptibility to social defeat stress; reduced Cacna1c expression in nucleus accumbens is causally associated with maladaptive outcomes after chronic social defeat. | Viral Cre-mediated conditional knockout in nucleus accumbens of floxed Cacna1c mice, social interaction and female urine preference assays | The international journal of neuropsychopharmacology | Medium | 28165117 |
| 2016 | Cacna1c forebrain knockout mice exhibit enhanced death of young hippocampal neurons (without change in NPC proliferation) and deficits in brain BDNF levels; adult hippocampal Cre-mediated knockdown of Cav1.2 recapitulates the survival deficit. | Forebrain-specific conditional knockout, BrdU/Ki67 labeling, TUNEL/survival assays, BDNF measurement, viral Cre knockdown in adults | eNeuro | Medium | 27066530 |
| 2018 | Cacna1c knockout specifically in serotonin (5-HT) neurons disrupts active-coping behavior in the forced swim test; this is rescued by blocking 5-HT1A receptors; Cacna1c knockout mice show enhanced Fos expression in caudal DR 5-HT neurons and enhanced response to a 5-HT1A antagonist in rostral DR neurons, indicating disrupted 5-HT neuron activation and 5-HT1A feedback inhibition. | 5-HT neuron-specific conditional Cacna1c knockout (temporally controlled), forced swim test, c-Fos immunohistochemistry, pharmacological rescue with WAY-100635 | Neuropharmacology | Medium | 30176250 |
| 2015 | Loss of Cav1.2 in the auditory brainstem (targeted embryonic deletion) causes significant decreases in auditory nuclei volume and cell number; action potentials of lateral superior olive neurons are narrower than controls; the medial nucleus of the trapezoid body undergoes rapid cell loss between P0 and P4. | Conditional knockout mouse, electrophysiology of auditory brainstem neurons, volumetric and cell-count analysis, auditory brainstem response recordings | The Journal of biological chemistry | Medium | 26242732 |
| 2023 | ANO1, CaV1.2, and IP3R co-assemble in a microdomain at or near the plasma membrane of pulmonary arterial smooth muscle cells (confirmed by co-immunoprecipitation and superresolution nanomicroscopy); this tripartite complex integrates stochastic Ca2+ release events and Ca2+ waves to sustain serotonin-induced arterial contraction. | Co-immunoprecipitation, confocal and superresolution microscopy, smooth muscle-specific ANO1 ablation, pharmacological blockade of CaV1.2 and IP3R, Ca2+ imaging with GCaMP | The Journal of general physiology | Medium | 37702787 |
| 2024 | In layer III pyramidal cells of dorsolateral prefrontal cortex, Cav1.2 (CACNA1C) is concentrated in dendritic spines near calcium-storing smooth ER, co-expressed with GRIN2B and KCNN3 (SK3); L-type calcium channel activation drives SK3-mediated inhibition of firing; both blockade and excessive activation of L-type channels reduce neuronal firing needed for working memory. | Electron and light microscopy of macaque dPFC, pharmacological blockade and activation of L-type channels during unit recording, working memory behavioral tasks, transcriptomic profiling of human and macaque pyramidal cells | JAMA psychiatry | Medium | 38776078 |
| 1991 | The human CACNA1C gene (encoding the α1 subunit of the cardiac dihydropyridine-sensitive Ca2+ channel, CCHL1A1) was mapped to chromosome 12p12-pter by PCR analysis of somatic cell hybrids. | PCR of human-rodent somatic cell hybrids with human-specific oligonucleotides | Genomics | Medium | 1653763 |
| Year | Title | Journal | Citations | PMID |
|---|---|---|---|---|
| 2001 | A beta2 adrenergic receptor signaling complex assembled with the Ca2+ channel Cav1.2. | Science (New York, N.Y.) | 441 | 11441182 |
| 2005 | Role of hippocampal Cav1.2 Ca2+ channels in NMDA receptor-independent synaptic plasticity and spatial memory. | The Journal of neuroscience : the official journal of the Society for Neuroscience | 357 | 16251435 |
| 2014 | L-type CaV1.2 calcium channels: from in vitro findings to in vivo function. | Physiological reviews | 285 | 24382889 |
| 2012 | CACNA1C (Cav1.2) in the pathophysiology of psychiatric disease. | Progress in neurobiology | 226 | 22705413 |
| 2011 | BIN1 is reduced and Cav1.2 trafficking is impaired in human failing cardiomyocytes. | Heart rhythm | 136 | 22138472 |
| 2017 | Cross-disorder risk gene CACNA1C differentially modulates susceptibility to psychiatric disorders during development and adulthood. | Molecular psychiatry | 125 | 28696432 |
| 2013 | MIR137 gene and target gene CACNA1C of miR-137 contribute to schizophrenia susceptibility in Han Chinese. | Schizophrenia research | 123 | 24275578 |
| 2018 | CACNA1C: Association With Psychiatric Disorders, Behavior, and Neurogenesis. | Schizophrenia bulletin | 119 | 29982775 |
| 2010 | CaV1.2 beta-subunit coordinates CaMKII-triggered cardiomyocyte death and afterdepolarizations. | Proceedings of the National Academy of Sciences of the United States of America | 106 | 20194790 |
| 2004 | Ser1928 is a common site for Cav1.2 phosphorylation by protein kinase C isoforms. | The Journal of biological chemistry | 101 | 15509562 |
| 2005 | Splicing for alternative structures of Cav1.2 Ca2+ channels in cardiac and smooth muscles. | Cardiovascular research | 100 | 16051206 |
| 2007 | Protein kinase G phosphorylates Cav1.2 alpha1c and beta2 subunits. | Circulation research | 95 | 17626895 |
| 2004 | Ca2+-binding protein-1 facilitates and forms a postsynaptic complex with Cav1.2 (L-type) Ca2+ channels. | The Journal of neuroscience : the official journal of the Society for Neuroscience | 94 | 15140941 |
| 2010 | Calcium influx through Cav1.2 is a proximal signal for pathological cardiomyocyte hypertrophy. | Journal of molecular and cellular cardiology | 92 | 21111744 |
| 2004 | An essential role of Cav1.2 L-type calcium channel for urinary bladder function. | FASEB journal : official publication of the Federation of American Societies for Experimental Biology | 89 | 15132976 |
| 2014 | Long QT syndrome type 8: novel CACNA1C mutations causing QT prolongation and variant phenotypes. | Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology | 79 | 24728418 |
| 2003 | Apocalmodulin and Ca2+ calmodulin-binding sites on the CaV1.2 channel. | Biophysical journal | 78 | 12944271 |
| 2009 | CaV1.2 channelopathies: from arrhythmias to autism, bipolar disorder, and immunodeficiency. | Pflugers Archiv : European journal of physiology | 77 | 19916019 |
| 2012 | CaV1.2 signaling complexes in the heart. | Journal of molecular and cellular cardiology | 73 | 23266596 |
| 2009 | Smooth muscle cell alpha2delta-1 subunits are essential for vasoregulation by CaV1.2 channels. | Circulation research | 69 | 19797702 |
| 2014 | Basal and β-adrenergic regulation of the cardiac calcium channel CaV1.2 requires phosphorylation of serine 1700. | Proceedings of the National Academy of Sciences of the United States of America | 66 | 25368181 |
| 2009 | Developmental control of CaV1.2 L-type calcium channel splicing by Fox proteins. | Molecular and cellular biology | 66 | 19564422 |
| 2010 | Mitochondria control functional CaV1.2 expression in smooth muscle cells of cerebral arteries. | Circulation research | 62 | 20616314 |
| 2016 | Phosphorylation of Cav1.2 on S1928 uncouples the L-type Ca2+ channel from the β2 adrenergic receptor. | The EMBO journal | 61 | 27103070 |
| 2013 | Calcium influx through L-type CaV1.2 Ca2+ channels regulates mandibular development. | The Journal of clinical investigation | 61 | 23549079 |
| 2018 | Postsynaptic localization and regulation of AMPA receptors and Cav1.2 by β2 adrenergic receptor/PKA and Ca2+/CaMKII signaling. | The EMBO journal | 57 | 30249603 |
| 2003 | Enhanced expression of L-type Cav1.3 calcium channels in murine embryonic hearts from Cav1.2-deficient mice. | The Journal of biological chemistry | 57 | 12900400 |
| 2015 | Calcium Signaling Pathway Genes RUNX2 and CACNA1C Are Associated With Calcific Aortic Valve Disease. | Circulation. Cardiovascular genetics | 56 | 26553695 |
| 2015 | MiR-103 inhibits osteoblast proliferation mainly through suppressing Cav1.2 expression in simulated microgravity. | Bone | 53 | 25868801 |
| 2013 | CACNA1C, schizophrenia and major depressive disorder in the Han Chinese population. | The British journal of psychiatry : the journal of mental science | 53 | 24262814 |
| 2019 | Cardiac CaV1.2 channels require β subunits for β-adrenergic-mediated modulation but not trafficking. | The Journal of clinical investigation | 52 | 30422117 |
| 2019 | TDP-43 regulates early-phase insulin secretion via CaV1.2-mediated exocytosis in islets. | The Journal of clinical investigation | 52 | 31355778 |
| 2016 | Cacna1c in the Prefrontal Cortex Regulates Depression-Related Behaviors via REDD1. | Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology | 52 | 27922594 |
| 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 |
| 2009 | PIKfyve regulates CaV1.2 degradation and prevents excitotoxic cell death. | The Journal of cell biology | 52 | 19841139 |
| 2016 | The Neuropsychiatric Disease-Associated Gene cacna1c Mediates Survival of Young Hippocampal Neurons. | eNeuro | 51 | 27066530 |
| 2009 | CACNA1C gene polymorphisms, cardiovascular disease outcomes, and treatment response. | Circulation. Cardiovascular genetics | 51 | 20031608 |
| 2010 | Molecular mechanisms, and selective pharmacological rescue, of Rem-inhibited CaV1.2 channels in heart. | Circulation research | 50 | 20616312 |
| 2018 | Cacna1c haploinsufficiency leads to pro-social 50-kHz ultrasonic communication deficits in rats. | Disease models & mechanisms | 47 | 29739816 |
| 2016 | Cav1.2 and Cav1.3 L-type calcium channels independently control short- and long-term sensitization to pain. | The Journal of physiology | 46 | 27231046 |
| 2012 | CaV1.2 sparklets in heart and vascular smooth muscle. | Journal of molecular and cellular cardiology | 46 | 23220157 |
| 2013 | CaV1.2 calcium channel expression in reactive astrocytes is associated with the formation of amyloid-β plaques in an Alzheimer's disease mouse model. | Journal of Alzheimer's disease : JAD | 45 | 23948887 |
| 2010 | Analysis of Cav1.2 and ryanodine receptor clusters in rat ventricular myocytes. | Biophysical journal | 43 | 21156134 |
| 2020 | Disruption of Cav1.2-mediated signaling is a pathway for ketamine-induced pathology. | Nature communications | 42 | 32859919 |
| 2019 | Estrogen receptor α promotes Cav1.2 ubiquitination and degradation in neuronal cells and in APP/PS1 mice. | Aging cell | 40 | 31012223 |
| 2015 | CaV1.2/CaV3.x channels mediate divergent vasomotor responses in human cerebral arteries. | The Journal of general physiology | 40 | 25918359 |
| 2017 | Increased Ca2+ signaling through CaV1.2 promotes bone formation and prevents estrogen deficiency-induced bone loss. | JCI insight | 39 | 29202453 |
| 2016 | CACNA1C hypermethylation is associated with bipolar disorder. | Translational psychiatry | 39 | 27271857 |
| 2016 | Common variants in CACNA1C and MDD susceptibility: A comprehensive meta-analysis. | American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics | 36 | 27260792 |
| 2011 | ANK3, CACNA1C and ZNF804A gene variants in bipolar disorders and psychosis subphenotype. | The world journal of biological psychiatry : the official journal of the World Federation of Societies of Biological Psychiatry | 36 | 21767209 |
| 2013 | Further evidence for genetic association of CACNA1C and schizophrenia: new risk loci in a Han Chinese population and a meta-analysis. | Schizophrenia research | 35 | 24355530 |
| 2015 | Genetic analysis of SNPs in CACNA1C and ANK3 gene with schizophrenia: A comprehensive meta-analysis. | American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics | 33 | 26227746 |
| 2013 | Protein kinase C-dependent activation of CaV1.2 channels selectively controls human TH2-lymphocyte functions. | The Journal of allergy and clinical immunology | 33 | 24365142 |
| 2008 | CaV1.2 rather than CaV1.3 is coupled to glucose-stimulated insulin secretion in INS-1 832/13 cells. | Journal of molecular endocrinology | 33 | 18562674 |
| 2006 | Coexpression of voltage-dependent calcium channels Cav1.2, 2.1a, and 2.1b in vascular myocytes. | Hypertension (Dallas, Tex. : 1979) | 33 | 16505211 |
| 2020 | Cav1.2 channelopathies causing autism: new hallmarks on Timothy syndrome. | Pflugers Archiv : European journal of physiology | 31 | 32621084 |
| 2017 | Decreased Nucleus Accumbens Expression of Psychiatric Disorder Risk Gene Cacna1c Promotes Susceptibility to Social Stress. | The international journal of neuropsychopharmacology | 31 | 28165117 |
| 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 |
| 2024 | Key Roles of CACNA1C/Cav1.2 and CALB1/Calbindin in Prefrontal Neurons Altered in Cognitive Disorders. | JAMA psychiatry | 30 | 38776078 |
| 2019 | CACNA1C (rs1006737) may be a susceptibility gene for schizophrenia: An updated meta-analysis. | Brain and behavior | 29 | 31033230 |
| 2018 | β-Subunit of the voltage-gated Ca2+ channel Cav1.2 drives signaling to the nucleus via H-Ras. | Proceedings of the National Academy of Sciences of the United States of America | 29 | 30150369 |
| 2015 | Homer proteins mediate the interaction between STIM1 and Cav1.2 channels. | Biochimica et biophysica acta | 29 | 25712868 |
| 2007 | Regulation of Cav1.2 current: interaction with intracellular molecules. | Journal of pharmacological sciences | 29 | 17409629 |
| 2019 | miR-221 and -222 target CACNA1C and KCNJ5 leading to altered cardiac ion channel expression and current density. | Cellular and molecular life sciences : CMLS | 28 | 31312877 |
| 2010 | Spatial association of the Cav1.2 calcium channel with α5β1-integrin. | American journal of physiology. Cell physiology | 28 | 21178109 |
| 2021 | Inhibiting microRNA-155 attenuates atrial fibrillation by targeting CACNA1C. | Journal of molecular and cellular cardiology | 26 | 33636223 |
| 2015 | Cacna1c (Cav1.2) Modulates Electroencephalographic Rhythm and Rapid Eye Movement Sleep Recovery. | Sleep | 26 | 25845695 |
| 2013 | State-dependent signaling by Cav1.2 regulates hair follicle stem cell function. | Genes & development | 26 | 23752588 |
| 2023 | CACNA1C-Related Channelopathies. | Handbook of experimental pharmacology | 25 | 36598608 |
| 1991 | Assignment of the human gene for the alpha 1 subunit of the cardiac DHP-sensitive Ca2+ channel (CCHL1A1) to chromosome 12p12-pter. | Genomics | 25 | 1653763 |
| 2020 | Dopamine D1R-neuron cacna1c deficiency: a new model of extinction therapy-resistant post-traumatic stress. | Molecular psychiatry | 24 | 32332995 |
| 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 |
| 2023 | ANO1, CaV1.2, and IP3R form a localized unit of EC-coupling in mouse pulmonary arterial smooth muscle. | The Journal of general physiology | 21 | 37702787 |
| 2022 | CACNA1C-AS2 inhibits cell proliferation and suppresses cell migration and invasion via targeting FBXO45 and PI3K/AKT/mTOR pathways in glioma. | Apoptosis : an international journal on programmed cell death | 21 | 36038736 |
| 2016 | NFAT5-mediated CACNA1C expression is critical for cardiac electrophysiological development and maturation. | Journal of molecular medicine (Berlin, Germany) | 21 | 27368804 |
| 2012 | ANK3 and CACNA1C--missing genetic link for bipolar disorder and major depressive disorder in two German case-control samples. | Journal of psychiatric research | 21 | 22647524 |
| 2022 | Bipolar-associated miR-499-5p controls neuroplasticity by downregulating the Cav1.2 subunit CACNB2. | EMBO reports | 20 | 35969184 |
| 2015 | CACNA1C gene and schizophrenia: a case-control and pharmacogenetic study. | Psychiatric genetics | 20 | 26049408 |
| 2024 | CardioDPi: An explainable deep-learning model for identifying cardiotoxic chemicals targeting hERG, Cav1.2, and Nav1.5 channels. | Journal of hazardous materials | 19 | 38805819 |
| 2022 | CaV1.2 channelopathic mutations evoke diverse pathophysiological mechanisms. | The Journal of general physiology | 19 | 36167061 |
| 2019 | Genetic Variation in the Psychiatric Risk Gene CACNA1C Modulates Reversal Learning Across Species. | Schizophrenia bulletin | 19 | 30304534 |
| 2018 | Cav1.2 L-type calcium channels regulate stress coping behavior via serotonin neurons. | Neuropharmacology | 19 | 30176250 |
| 2017 | Genes Involved in Neurodevelopment, Neuroplasticity, and Bipolar Disorder: CACNA1C, CHRNA1, and MAPK1. | Neuropsychobiology | 19 | 28494468 |
| 2015 | L-type Calcium Channel Cav1.2 Is Required for Maintenance of Auditory Brainstem Nuclei. | The Journal of biological chemistry | 19 | 26242732 |
| 2020 | Vasorelaxing Activity of R-(-)-3'-Hydroxy-2,4,5-trimethoxydalbergiquinol from Dalbergia tonkinensis: Involvement of Smooth Muscle CaV1.2 Channels. | Planta medica | 18 | 31994147 |
| 2009 | Silencing of Cav1.2 gene in neonatal cardiomyocytes by lentiviral delivered shRNA. | Biochemical and biophysical research communications | 18 | 19422800 |
| 2023 | Regulation of Cardiac Cav1.2 Channels by Calmodulin. | International journal of molecular sciences | 17 | 37047381 |
| 2022 | Antenatal Dexamethasone Exposure Impairs Vascular Contractile Functions via Upregulating IP3 Receptor 1 and Cav1.2 in Adult Male Offspring. | Hypertension (Dallas, Tex. : 1979) | 17 | 35762340 |
| 2021 | Effects of clozapine and risperidone antipsychotic drugs on the expression of CACNA1C and behavioral changes in rat 'Ketamine model of schizophrenia. | Neuroscience letters | 17 | 34801642 |
| 2019 | CACNA1C polymorphism and brain cortical structure in bipolar disorder. | Journal of psychiatry & neuroscience : JPN | 17 | 31829002 |
| 2017 | A mutation in the CACNA1C gene leads to early repolarization syndrome with incomplete penetrance: A Chinese family study. | PloS one | 17 | 28493952 |
| 2016 | Resistance to pathologic cardiac hypertrophy and reduced expression of CaV1.2 in Trpc3-depleted mice. | Molecular and cellular biochemistry | 17 | 27522668 |
| 2015 | CACNA1C polymorphism and altered phosphorylation of tau in bipolar disorder. | The British journal of psychiatry : the journal of mental science | 17 | 26541689 |
| 2022 | Role of CACNA1C in Brugada syndrome: Prevalence and phenotype of probands referred for genetic testing. | Heart rhythm | 16 | 34999275 |
| 2022 | Huntington-associated protein 1 inhibition contributes to neuropathic pain by suppressing Cav1.2 activity and attenuating inflammation. | Pain | 16 | 36508175 |
| 2009 | Transcriptional and electrophysiological consequences of KChIP2-mediated regulation of CaV1.2. | Channels (Austin, Tex.) | 16 | 19713767 |
| 2020 | The genome-wide supported CACNA1C gene polymorphisms and the risk of schizophrenia: an updated meta-analysis. | BMC medical genetics | 15 | 32770953 |
| 2019 | Dysfunctional Cav1.2 channel in Timothy syndrome, from cell to bedside. | Experimental biology and medicine (Maywood, N.J.) | 15 | 31324123 |
| 2016 | Rab25 influences functional Cav1.2 channel surface expression in arterial smooth muscle cells. | American journal of physiology. Cell physiology | 15 | 27076616 |
| 2015 | Evaluating the association between CACNA1C rs1006737 and schizophrenia risk: A meta-analysis. | Asia-Pacific psychiatry : official journal of the Pacific Rim College of Psychiatrists | 15 | 25588813 |
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