CACNA1H

Summary

Gene Symbol: CACNA1H
Description: calcium voltage-gated channel subunit alpha1 H
Alias: CACNA1HB, Cav3.2, ECA6, EIG6, HALD4, voltage-dependent T-type calcium channel subunit alpha-1H, calcium channel, voltage-dependent, T type, alpha 1H subunit, calcium channel, voltage-dependent, T type, alpha 1Hb subunit, low-voltage-activated calcium channel alpha1 3.2 subunit, low-voltage-activated calcium channel alpha13.2 subunit, voltage dependent t-type calcium channel alpha-1H subunit, voltage-gated calcium channel alpha subunit Cav3.2, voltage-gated calcium channel alpha subunit CavT.2, voltage-gated calcium channel subunit alpha Cav3.2
Species: human
Products:     CACNA1H

Top Publications

  1. Cribbs L, Lee J, Yang J, Satin J, Zhang Y, Daud A, et al. Cloning and characterization of alpha1H from human heart, a member of the T-type Ca2+ channel gene family. Circ Res. 1998;83:103-9 pubmed
    ..We mapped the gene, CACNA1H, to human chromosome 16p13.3 and mouse chromosome 17...
  2. Mariot P, Vanoverberghe K, Lalevee N, Rossier M, Prevarskaya N. Overexpression of an alpha 1H (Cav3.2) T-type calcium channel during neuroendocrine differentiation of human prostate cancer cells. J Biol Chem. 2002;277:10824-33 pubmed
    ..This voltage-dependent calcium channel could be involved in the stimulation of mitogenic factor secretion and could therefore be a target for future therapeutic strategies. ..
  3. Kang H, Park J, Jeong S, Kim J, Moon H, Perez Reyes E, et al. A molecular determinant of nickel inhibition in Cav3.2 T-type calcium channels. J Biol Chem. 2006;281:4823-30 pubmed
    ..1. These findings indicate that His-191 in the S3-S4 loop is a critical residue conferring nickel block to Ca(v)3.2 and reveal a novel role for the S3-S4 loop to control ion permeation through T-type Ca2+ channels. ..
  4. Catterall W, Perez Reyes E, Snutch T, Striessnig J. International Union of Pharmacology. XLVIII. Nomenclature and structure-function relationships of voltage-gated calcium channels. Pharmacol Rev. 2005;57:411-25 pubmed
    ..This article presents the molecular relationships and physiological functions of these calcium channel proteins and provides comprehensive information on their molecular, genetic, physiological, and pharmacological properties. ..
  5. Chen C, Lamping K, Nuno D, Barresi R, Prouty S, Lavoie J, et al. Abnormal coronary function in mice deficient in alpha1H T-type Ca2+ channels. Science. 2003;302:1416-8 pubmed
    ..Furthermore, acute blockade of T-channels with Ni2+ prevented relaxation of wild-type coronary arteries. Thus, Ca2+ influx through alpha1H T-type Ca2+ channels is essential for normal relaxation of coronary arteries. ..
  6. He Y, Gao Q, Han B, Zhu X, Zhu D, Tao J, et al. Progesterone suppressed vasoconstriction in human umbilical vein via reducing calcium entry. Steroids. 2016;108:118-25 pubmed publisher
  7. Buckley M, O Halloran K, Rae M, Dinan T, O Malley D. Modulation of enteric neurons by interleukin-6 and corticotropin-releasing factor contributes to visceral hypersensitivity and altered colonic motility in a rat model of irritable bowel syndrome. J Physiol. 2014;592:5235-50 pubmed publisher
    ..Moreover, combined targeting of peripheral IL-6 and CRF1 receptors is effective in alleviating IBS-like symptoms in the WKY rat. Thus, crosstalk between stress and immune factors during IBS flares may underlie symptom exacerbation. ..
  8. Zhang Y, Qin W, Qian Z, Liu X, Wang H, Gong S, et al. Peripheral pain is enhanced by insulin-like growth factor 1 through a G protein-mediated stimulation of T-type calcium channels. Sci Signal. 2014;7:ra94 pubmed publisher
  9. Marks W, Cain S, Snutch T, Howland J. The T-type calcium channel antagonist Z944 rescues impairments in crossmodal and visual recognition memory in Genetic Absence Epilepsy Rats from Strasbourg. Neurobiol Dis. 2016;94:106-15 pubmed publisher
    ..Future research into the therapeutic potential of T-type calcium channel regulation may be particularly fruitful for the treatment of CAE and other disorders characterized by visual memory deficits. ..

More Information

Publications123 found, 100 shown here

  1. Dong L, Cheng X, Zhou L, Hu Y. Calcium channels are involved in EphB/ephrinB reverse signaling?induced apoptosis in a rat chronic ocular hypertension model. Mol Med Rep. 2017;: pubmed publisher
    ..Thus, the results suggest that Ca2+ channels in a COH model may be a pathway involved in ephrinB/EphB signaling?induced RGC apoptosis...
  2. Thevenod F. Catch me if you can! Novel aspects of cadmium transport in mammalian cells. Biometals. 2010;23:857-75 pubmed publisher
  3. Sharop B, Boldyriev O, Batiuk M, Shtefan N, Shuba Y. Compensatory reduction of Cav3.1 expression in thalamocortical neurons of juvenile rats of WAG/Rij model of absence epilepsy. Epilepsy Res. 2016;119:10-2 pubmed publisher
    ..The weakened expression of Cav3.1 in juveniles of WAG/Rij rats could represent a compensatory mechanism determining the pattern of the age dependency in the disease manifestation by this model of absence epilepsy. ..
  4. Powell K, Tang H, Ng C, Guillemain I, Dieuset G, Dezsi G, et al. Seizure expression, behavior, and brain morphology differences in colonies of Genetic Absence Epilepsy Rats from Strasbourg. Epilepsia. 2014;55:1959-68 pubmed publisher
    ..A previously identified mutation in the Cacna1h gene controlling the CaV 3...
  5. Korah H, Scholl U. An Update on Familial Hyperaldosteronism. Horm Metab Res. 2015;47:941-6 pubmed publisher
    ..In contrast, a recent exome sequencing study identified germline mutations in CACNA1H (a T-type calcium channel), previously undescribed in adenomas, in 5 unrelated families with early-onset primary ..
  6. Huang I, Hsu Y, Chen C, Chen M, Wen Z, Huang H, et al. Excavatolide-B Enhances Contextual Memory Retrieval via Repressing the Delayed Rectifier Potassium Current in the Hippocampus. Mar Drugs. 2018;16: pubmed publisher
    ..The human CACNA1H gene encodes a T-type calcium channel (Cav3...
  7. Cabahug Zuckerman P, Stout R, Majeska R, Thi M, Spray D, Weinbaum S, et al. Potential Role for a Specialized ?3 Integrin-Based Structure On Osteocyte Processes in Bone Mechanosensation. J Orthop Res. 2017;: pubmed publisher
    ..These findings identify a possible structural basis for the unique mechanosensation and transduction capabilities of the osteocyte process. This article is protected by copyright. All rights reserved...
  8. Sakkaki S, Gangarossa G, Lerat B, Françon D, Forichon L, Chemin J, et al. Blockade of T-type calcium channels prevents tonic-clonic seizures in a maximal electroshock seizure model. Neuropharmacology. 2016;101:320-9 pubmed publisher
    ..Overall, our data indicate that TTA-A2 is a potent anticonvulsant and that the Cav3.1 isoform plays a prominent role in mediating TTA-A2 tonic seizure protection. ..
  9. Bladen C, McDaniel S, Gadotti V, Petrov R, Berger N, Diaz P, et al. Characterization of novel cannabinoid based T-type calcium channel blockers with analgesic effects. ACS Chem Neurosci. 2015;6:277-87 pubmed publisher
    ..Taken together, our data reveal a novel class of compounds whose physiological and therapeutic actions are mediated through block of Cav3.2 calcium channels. ..
  10. Stemkowski P, García Caballero A, Gadotti V, M Dahoma S, Huang S, Black S, et al. TRPV1 Nociceptor Activity Initiates USP5/T-type Channel-Mediated Plasticity. Cell Rep. 2016;17:2901-2912 pubmed publisher
    ..2 channel activity. This neuronal-activity-induced USP5 upregulation may underlie a protective, transient sensitization of the pain pathway. ..
  11. Schaller D, Gunduz M, Zhang F, Zamponi G, Wolber G. Binding mechanism investigations guiding the synthesis of novel condensed 1,4-dihydropyridine derivatives with L-/T-type calcium channel blocking activity. Eur J Med Chem. 2018;155:1-12 pubmed publisher
    ..2. Additionally, we identified four compounds active against Cav3.2 of which three were selective over Cav1.2. Novel binding modes were analyzed using docking and pharmacophore analysis as well as molecular dynamics simulations. ..
  12. Fukami K, Asano E, Ueda M, Sekiguchi F, Yoshida S, Kawabata A. High glucose induces N-linked glycosylation-mediated functional upregulation and overexpression of Cav3.2 T-type calcium channels in neuroendocrine-like differentiated human prostate cancer cells. J Pharmacol Sci. 2017;133:57-60 pubmed publisher
    ..Hyperglycemia thus appears to induce N-linked glycosylation-mediated functional upregulation and overexpression of Cav3.2 in neuroendocrine-like differentiated prostate cancer cells. ..
  13. Pudukulatham Z, Zhang F, Gadotti V, M Dahoma S, Swami P, Tamboli Y, et al. Synthesis and characterization of a disubstituted piperazine derivative with T-type channel blocking action and analgesic properties. Mol Pain. 2016;12: pubmed publisher
    ..2 channels. Altogether, our data identify a novel T-type calcium channel blocker with tight structure activity relationship (SAR) and relevant in vivo efficacy in inflammatory pain conditions. ..
  14. Shen F, Chen Z, Zhong W, Ma L, Chen C, Yang Z, et al. Alleviation of neuropathic pain by regulating T-type calcium channels in rat anterior cingulate cortex. Mol Pain. 2015;11:7 pubmed publisher
    ..TCCs in the ACC may be contributing to the maintenance of neuropathic pain, and the neuropathic pain can be alleviated by inhibiting the neuronal activity of ACC through modulating the TCCs. ..
  15. Bezençon O, Remen L, Richard S, Roch C, Kessler M, Ertel E, et al. Discovery and evaluation of Cav3.2-selective T-type calcium channel blockers. Bioorg Med Chem Lett. 2017;27:5326-5331 pubmed publisher
    ..1- and Cav3.3-channels. These compounds display poor physicochemical and DMPK properties, making their use difficult for in vivo applications. Nevertheless, they are well-suited for in vitro studies. ..
  16. Teleb M, Rizk O, Zhang F, Fronczek F, Zamponi G, Fahmy H. Design, synthesis and pharmacological evaluation of some substituted dihydropyrimidines with L-/T-type calcium channel blocking activities. Bioorg Chem. 2018;83:354-366 pubmed publisher
    ..2. Their drug-likeness has been assessed using Molinspiration and Molsoft softwares. Their physicochemical properties and pharmacokinetic profiles recommend that they can be considered as drug-like candidates. ..
  17. Wang X, Tian B, Huang Y, Peng X, Chen L, Li J, et al. Corrigendum: Hydrogen sulfide-induced itch requires activation of Cav3.2 T-type calcium channel in mice. Sci Rep. 2017;7:46906 pubmed publisher
    ..This corrects the article DOI: 10.1038/srep16768...
  18. Felizola S, Katsu K, Ise K, Nakamura Y, Arai Y, Satoh F, et al. Pre-B Lymphocyte Protein 3 (VPREB3) Expression in the Adrenal Cortex: Precedent for non-Immunological Roles in Normal and Neoplastic Human Tissues. Endocr Pathol. 2015;26:119-28 pubmed publisher
    ..023; R = 0.31) and CaV3.2 (P = 0.0019; R = 0.42). Based on our data, we hypothesize a possible role for VPREB3 in aldosterone biosynthesis, and present ideas for future functional studies. ..
  19. Corney B, Widnall C, Rees D, Davies J, Crunelli V, Carter D. Regulatory Architecture of the Neuronal Cacng2/Tarpγ2 Gene Promoter: Multiple Repressive Domains, a Polymorphic Regulatory Short Tandem Repeat, and Bidirectional Organization with Co-regulated lncRNAs. J Mol Neurosci. 2019;67:282-294 pubmed publisher
    ..NEC difference, indicating that this specific STR length variation may only be relevant in the context of other (Cacna1h and Kcnk9) gene variants in this disease model...
  20. Ferdous Z, Qureshi M, Jayaprakash P, Parekh K, John A, Oz M, et al. Different Profile of mRNA Expression in Sinoatrial Node from Streptozotocin-Induced Diabetic Rat. PLoS ONE. 2016;11:e0153934 pubmed publisher
    ..membrane transport, Slc8a1, Trpc1, Trpc6 (4-fold); intracellular Ca2+-transport, Ryr3; calcium channel Cacna1g, Cacna1h, Cacnb3; potassium channels, Kcnj5, Kcnk3 and natriuretic peptides, Nppa (5-fold) and Nppb (7-fold)...
  21. Sundararajan T, Manzardo A, Butler M. Functional analysis of schizophrenia genes using GeneAnalytics program and integrated databases. Gene. 2018;641:25-34 pubmed publisher
    ..g., GABRA1, GABRB2), dopaminergic receptors (e.g., DRD1, DRD2), calcium-related channels (e.g., CACNA1H, CACNA1B), solute transporters (e.g., SLC1A1, SLC6A2) and for neurodevelopment (e.g...
  22. Tomášová L, Pavlovicová M, Malekova L, Misak A, Kristek F, Grman M, et al. Effects of AP39, a novel triphenylphosphonium derivatised anethole dithiolethione hydrogen sulfide donor, on rat haemodynamic parameters and chloride and calcium Cav3 and RyR2 channels. Nitric Oxide. 2015;46:131-44 pubmed publisher
  23. Liang J, Teoh N, Xu L, Pok S, Li X, Chu E, et al. Dietary cholesterol promotes steatohepatitis related hepatocellular carcinoma through dysregulated metabolism and calcium signaling. Nat Commun. 2018;9:4490 pubmed publisher
    ..genes (ALDH18A1, CAD, CHKA, POLD4, PSPH and SQLE) and recurrently mutated genes (RYR1, MTOR, SDK1, CACNA1H and RYR2)...
  24. Zennaro M, Jeunemaitre X. SFE/SFHTA/AFCE consensus on primary aldosteronism, part 5: Genetic diagnosis of primary aldosteronism. Ann Endocrinol (Paris). 2016;77:214-9 pubmed publisher
    ..Recently, a new autosomal-dominant form of familial PA, FH-IV, associated with mutations in the CACNA1H gene, was described in patients with hypertension and PA before the age of 10years...
  25. Terada Y, Tsubota M, Sugo H, Wakitani K, Sekiguchi F, Wada K, et al. Tacrolimus Triggers Transient Receptor Potential Vanilloid-1-Dependent Relapse of Pancreatitis-Related Pain in Mice. Pharmacology. 2017;99:281-285 pubmed publisher
    ..Thus, tacrolimus appears to cause the TRPV1-dependent relapse of pancreatitis-related pain, suggesting the involvement of calcineurin in the termination of pancreatic pain. ..
  26. Monticone S, Buffolo F, Tetti M, Veglio F, Pasini B, Mulatero P. GENETICS IN ENDOCRINOLOGY: The expanding genetic horizon of primary aldosteronism. Eur J Endocrinol. 2018;178:R101-R111 pubmed publisher
    ..Germline mutations in KCNJ5 and CACNA1H cause FH-III and FH-IV, respectively, while germline mutations in CACNA1D cause the rare PASNA ..
  27. Staehlke S, Koertge A, Nebe B. Intracellular calcium dynamics dependent on defined microtopographical features of titanium. Biomaterials. 2015;46:48-57 pubmed publisher
    ..The topography-dependent calcium dynamics observed here provide new insights into how topographical cues alter cell functions - via the intracellular Ca(2+) signaling. ..
  28. Neumaier F, Dibué Adjei M, Hescheler J, Schneider T. Voltage-gated calcium channels: Determinants of channel function and modulation by inorganic cations. Prog Neurobiol. 2015;129:1-36 pubmed publisher
    ..The fact that these ions can often traverse VGCCs can contribute to the detrimental intracellular accumulation of metal ions following excessive release of endogenous Cu(2+) and Zn(2+) or exposure to non-physiological toxic metal ions. ..
  29. Drumm B, Sung T, Zheng H, Baker S, KOH S, Sanders K. The effects of mitochondrial inhibitors on Ca2+ signalling and electrical conductances required for pacemaking in interstitial cells of Cajal in the mouse small intestine. Cell Calcium. 2018;72:1-17 pubmed publisher
    ..A direct obligatory role for mitochondria in pacemaker activity is therefore questionable. ..
  30. Fernandes Rosa F, Boulkroun S, Zennaro M. Somatic and inherited mutations in primary aldosteronism. J Mol Endocrinol. 2017;59:R47-R63 pubmed publisher
    ..The description of germline KCNJ5 and CACNA1H mutations has identified FH-III and FH-IV based on genetic findings; germline CACNA1D mutations have ..
  31. Martinello K, Huang Z, Lujan R, Tran B, Watanabe M, Cooper E, et al. Cholinergic afferent stimulation induces axonal function plasticity in adult hippocampal granule cells. Neuron. 2015;85:346-63 pubmed publisher
    ..Since alterations in axonal signaling affect neuronal firing patterns and neurotransmitter release, this is an unreported cellular mechanism by which acetylcholine might, at least partly, enhance cognitive processing. ..
  32. Shimaoka T, Wang Y, Morishima M, Miyamoto S, Ono K. Hypomagnesemic down-regulation of L-type Ca(2+) channel in cardiomyocyte as an arrhythmogenic substrate in rats. Pathophysiology. 2015;22:87-93 pubmed publisher
    ..2. These findings provide novel insights into hypomagnesemic electrophysiological disorders in the heart, and should be considered when assessing the design of effective antiarrhythmic treatments in patients with hypomagnesemia. ..
  33. Jeong K, Lee S, Seo H, Oh Y, Jang D, Choe J, et al. Ca-α1T, a fly T-type Ca2+ channel, negatively modulates sleep. Sci Rep. 2015;5:17893 pubmed publisher
    ..Thus, our study suggests invertebrate T-type Ca(2+) channels promote wakefulness rather than stabilizing sleep. ..
  34. Nagi S, Dunn J, Birznieks I, Vickery R, Mahns D. The effects of preferential A- and C-fibre blocks and T-type calcium channel antagonist on detection of low-force monofilaments in healthy human participants. BMC Neurosci. 2015;16:52 pubmed publisher
    ..Convergent findings in glabrous and hairy skin lend support for an underlying system of innocuous mechanoreception with Cav3.2-expressing unmyelinated fibres. ..
  35. Eckle V, Shcheglovitov A, Vitko I, Dey D, Yap C, Winckler B, et al. Mechanisms by which a CACNA1H mutation in epilepsy patients increases seizure susceptibility. J Physiol. 2014;592:795-809 pubmed publisher
    ..Mutations in the gene encoding Cav3.2 T-type Ca(2+) channels, CACNA1H, have been found in association with various forms of idiopathic generalized epilepsy...
  36. Liang J, Zhang Y, Chen Y, Wang J, Pan H, Wu H, et al. Common polymorphisms in the CACNA1H gene associated with childhood absence epilepsy in Chinese Han population. Ann Hum Genet. 2007;71:325-35 pubmed
    Variants with a relatively high frequency in the CACNA1H gene have previously been identified in cases of childhood absence epilepsy (CAE) in the Chinese Han population most of which are located in exons 6 to 12...
  37. Garcia Caballero A, Gadotti V, Chen L, Zamponi G. A cell-permeant peptide corresponding to the cUBP domain of USP5 reverses inflammatory and neuropathic pain. Mol Pain. 2016;12: pubmed publisher
    ..2 channels. Targeting the interaction of this region with the Cav3.2 channel can be exploited as the basis for therapeutic intervention into inflammatory and neuropathic pain. ..
  38. Fukami K, Sekiguchi F, Kawabata A. Hydrogen Sulfide and T-Type Ca2+ Channels in Pain Processing, Neuronal Differentiation and Neuroendocrine Secretion. Pharmacology. 2017;99:196-203 pubmed publisher
    ..Key Messages: The H2S/Cav3.2 pathway may serve as therapeutic targets for treatment of intractable pain, neuronal injury, androgen-independent prostate cancer, cardiovascular diseases, etc. ..
  39. Smith C, Abdallah S, Wong Y, Le P, Harracksingh A, Artinian L, et al. Evolutionary insights into T-type Ca2+ channel structure, function, and ion selectivity from the Trichoplax adhaerens homologue. J Gen Physiol. 2017;149:483-510 pubmed publisher
    ..TCav3 is the most divergent metazoan T-type calcium channel and thus provides an evolutionary perspective on Cav3 channel structure-function properties, ion selectivity, and cellular physiology. ..
  40. Bernal Sierra Y, Haseleu J, Kozlenkov A, Begay V, Lewin G. Genetic Tracing of Cav3.2 T-Type Calcium Channel Expression in the Peripheral Nervous System. Front Mol Neurosci. 2017;10:70 pubmed publisher
    ..A second population of nociceptive sensory neurons expressing the Cav3.2 gene was found to be positive for the calcitonin-gene related peptide but these neurons are deep tissue nociceptors that do not innervate the skin. ..
  41. Sekiguchi F, Kawara Y, Tsubota M, Kawakami E, Ozaki T, Kawaishi Y, et al. Therapeutic potential of RQ-00311651, a novel T-type Ca2+ channel blocker, in distinct rodent models for neuropathic and visceral pain. Pain. 2016;157:1655-65 pubmed publisher
    ..1/Cav3.2 T channels and may serve as an orally available analgesic for treatment of neuropathic and inflammatory pain including distinct visceral pain with minimum central side effects. ..
  42. Ijjaali I, Barrere C, Nargeot J, Petitet F, Bourinet E. Ligand-based virtual screening to identify new T-type calcium channel blockers. Channels (Austin). 2007;1:300-4 pubmed
    ..2 mediated T-type current. Two series of compounds show chemical originality compared with known T-type calcium channel blockers. ..
  43. Mor M, Beharier O, Levy S, Kahn J, Dror S, Blumenthal D, et al. ZnT-1 enhances the activity and surface expression of T-type calcium channels through activation of Ras-ERK signaling. Am J Physiol Cell Physiol. 2012;303:C192-203 pubmed publisher
    ..1 and CaV3.2 through activation of Ras-ERK signaling. The augmentation of CaV3.1 currents by Ras-ERK activation is associated with enhanced trafficking of the channel to the plasma membrane. ..
  44. Huang C, Chen Y, Chen C. Physical interaction between calcineurin and Cav3.2 T-type Ca2+ channel modulates their functions. FEBS Lett. 2013;587:1723-30 pubmed publisher
    ..2 regulates calcineurin/NFAT pathway through both the Ca(2+) influx and calcineurin binding. Our findings unveiled a reciprocal regulation of Ca(2+) signaling which contributes to our understanding of cardiac hypertrophy. ..
  45. Park S, Min S, Kang H, Lee J. Differential zinc permeation and blockade of L-type Ca2+ channel isoforms Cav1.2 and Cav1.3. Biochim Biophys Acta. 2015;1848:2092-100 pubmed publisher
    ..2. In overall, we provide evidence that Cav1.2 and Cav1.3 isoforms are capable of potentially functioning as zinc permeation routes, through which zinc entry can be differentially augmented by mild acidifications. ..
  46. Aromolaran K, Benzow K, Cribbs L, Koob M, Piedras Rentería E. T-type current modulation by the actin-binding protein Kelch-like 1. Am J Physiol Cell Physiol. 2010;298:C1353-62 pubmed publisher
    ..This constitutes a novel regulatory mechanism of T-type calcium currents and supports the role of KLHL1 in the modulation of cellular excitability. ..
  47. Rehak R, Bartoletti T, Engbers J, Berecki G, Turner R, Zamponi G. Low voltage activation of KCa1.1 current by Cav3-KCa1.1 complexes. PLoS ONE. 2013;8:e61844 pubmed publisher
    ..1 activation over a wide range of membrane potentials according to the unique voltage profile of Cav3 calcium channels, greatly extending the roles for KCa1.1 potassium channels in controlling membrane excitability. ..
  48. Sekiguchi F, Miyamoto Y, Kanaoka D, Ide H, Yoshida S, Ohkubo T, et al. Endogenous and exogenous hydrogen sulfide facilitates T-type calcium channel currents in Cav3.2-expressing HEK293 cells. Biochem Biophys Res Commun. 2014;445:225-9 pubmed publisher
    ..2-HEK293 cells, and that exogenous H2S is capable of enhancing Cav3.2 function when endogenous H2S production by CSE is inhibited. In addition, Na2S is considered a more potent H2S donor than NaHS in vitro as well as in vivo. ..
  49. Harraz O, Brett S, Zechariah A, Romero M, Puglisi J, Wilson S, et al. Genetic ablation of CaV3.2 channels enhances the arterial myogenic response by modulating the RyR-BKCa axis. Arterioscler Thromb Vasc Biol. 2015;35:1843-51 pubmed publisher
    ..2(-/-) and wild-type animals were similar. Overall, our findings establish a negative feedback mechanism of the myogenic response in which CaV3.2 channel modulates downstream ryanodine receptor-BKCa to hyperpolarize and relax arteries. ..
  50. Bijlenga P, Liu J, Espinos E, Haenggeli C, Fischer Lougheed J, Bader C, et al. T-type alpha 1H Ca2+ channels are involved in Ca2+ signaling during terminal differentiation (fusion) of human myoblasts. Proc Natl Acad Sci U S A. 2000;97:7627-32 pubmed
    ..A similar mechanism could operate in other cell types of which differentiation implicates membrane hyperpolarization. ..
  51. DePuy S, Yao J, Hu C, McIntire W, Bidaud I, Lory P, et al. The molecular basis for T-type Ca2+ channel inhibition by G protein beta2gamma2 subunits. Proc Natl Acad Sci U S A. 2006;103:14590-5 pubmed
    ..These amino acids on the beta-torus identify a region that is distinct from those regions that contact the Galpha subunit or other effectors. ..
  52. Weiss N, Lacinova L. T-type channels: release a brake, engage a gear. Channels (Austin). 2016;10:78-80 pubmed publisher
  53. Ozaki T, Matsuoka J, Tsubota M, Tomita S, Sekiguchi F, Minami T, et al. Zinc deficiency promotes cystitis-related bladder pain by enhancing function and expression of Cav3.2 in mice. Toxicology. 2018;393:102-112 pubmed publisher
    ..2 in nociceptors, suggesting a novel therapeutic avenue for treatment of bladder pain, such as zinc supplementation. ..
  54. Scholl U, Stölting G, Nelson Williams C, Vichot A, Choi M, Loring E, et al. Recurrent gain of function mutation in calcium channel CACNA1H causes early-onset hypertension with primary aldosteronism. elife. 2015;4:e06315 pubmed publisher
    ..Five subjects (12.5%) shared the identical, previously unidentified, heterozygous CACNA1H(M1549V) mutation. Two mutations were demonstrated to be de novo events, and all mutations occurred independently...
  55. Huang D, Liang C, Zhang F, Men H, Du X, Gamper N, et al. Inflammatory mediator bradykinin increases population of sensory neurons expressing functional T-type Ca(2+) channels. Biochem Biophys Res Commun. 2016;473:396-402 pubmed publisher
    ..2 channels, particularly in neurons that do not display measurable LVA currents under control conditions. ..
  56. Sekiguchi F, Kawabata A. T-type calcium channels: functional regulation and implication in pain signaling. J Pharmacol Sci. 2013;122:244-50 pubmed
    ..Thus, Cav3.2 T-channels are considered to serve as novel targets for development of drugs for treatment of intractable pain resistant to currently available analgesics. ..
  57. Monteil A, Chausson P, Boutourlinsky K, Mezghrani A, Huc Brandt S, Blesneac I, et al. Inhibition of Cav3.2 T-type Calcium Channels by Its Intracellular I-II Loop. J Biol Chem. 2015;290:16168-76 pubmed publisher
    ..2 and Cav3.3 channels, only the fast inactivating T-type current (Cav3.2 component) was significantly inhibited. Altogether, these data describe a new strategy to differentially inhibit Cav3 isoforms of the T-type calcium channels. ..
  58. Glauser T, Holland K, O Brien V, Keddache M, Martin L, Clark P, et al. Pharmacogenetics of antiepileptic drug efficacy in childhood absence epilepsy. Ann Neurol. 2017;81:444-453 pubmed publisher
    To determine whether common polymorphisms in CACNA1G, CACNA1H, CACNA1I, and ABCB1 are associated with differential short-term seizure outcome in childhood absence epilepsy (CAE)...
  59. M Dahoma S, Gadotti V, Zhang F, Park B, Nam J, Onnis V, et al. Effect of the T-type channel blocker KYS-05090S in mouse models of acute and neuropathic pain. Pflugers Arch. 2016;468:193-9 pubmed publisher
    ..Those results indicate that KYS-05090S mediates a potent analgesic effect in inflammatory and neuropathic pain through T-type channel modulation, suggesting that its scaffold could be explored as a new class of analgesic compounds. ..
  60. Henbid M, Marks W, Collins M, Cain S, Snutch T, Howland J. Sociability impairments in Genetic Absence Epilepsy Rats from Strasbourg: Reversal by the T-type calcium channel antagonist Z944. Exp Neurol. 2017;296:16-22 pubmed publisher
    ..Future research should focus on T-type calcium channels in the treatment of sociability deficits observed in disorders such as CAE. ..
  61. Stemkowski P, Garcia Caballero A, Gadotti V, M Dahoma S, Chen L, Souza I, et al. Identification of interleukin-1 beta as a key mediator in the upregulation of Cav3.2-USP5 interactions in the pain pathway. Mol Pain. 2017;13:1744806917724698 pubmed publisher
    ..2 channels in the pain pathway, presumably by triggering increased firing activity in afferent fibers. ..
  62. Wang X, Tian B, Huang Y, Peng X, Chen L, Li J, et al. Hydrogen sulfide-induced itch requires activation of Cav3.2 T-type calcium channel in mice. Sci Rep. 2015;5:16768 pubmed publisher
    ..These results indicated that H2S, as a novel nonhistaminergic itch mediator, may activates Cav3.2 T-type calcium channel, probably located at A-fibers, to induce scratching and alloknesis in mice. ..
  63. Crunelli V, Toth T, Cope D, Blethyn K, Hughes S. The 'window' T-type calcium current in brain dynamics of different behavioural states. J Physiol. 2005;562:121-9 pubmed
  64. Zhong X, Liu J, Kyle J, Hanck D, Agnew W. A profile of alternative RNA splicing and transcript variation of CACNA1H, a human T-channel gene candidate for idiopathic generalized epilepsies. Hum Mol Genet. 2006;15:1497-512 pubmed
    ..b>CACNA1H is a human gene encoding Ca(v)3...
  65. Somekawa S, Imagawa K, Naya N, Takemoto Y, Onoue K, Okayama S, et al. Regulation of aldosterone and cortisol production by the transcriptional repressor neuron restrictive silencer factor. Endocrinology. 2009;150:3110-7 pubmed publisher
    ..We found a NRSE-like sequence in human CYP11B2 and CYP11B1 genes as well as the CACNA1H gene of many mammalian species. The CACNA1H gene encodes the alpha-subunit of Cav3.2...
  66. Ohkubo T, Yamazaki J. T-type voltage-activated calcium channel Cav3.1, but not Cav3.2, is involved in the inhibition of proliferation and apoptosis in MCF-7 human breast cancer cells. Int J Oncol. 2012;41:267-75 pubmed publisher
    ..1 knockdown blocked cyclophosphamide-induced apoptosis. These results suggest that Cav3.1 channels may contribute to the repression of tumor proliferation and the promotion of apoptosis mediated via Cav3.1-specific Ca2+ influx. ..
  67. Wang S, Wang P, Gao F, Li Q, Liu Z, Fu X, et al. [Decreased mRNA expressions of T-type channel alpha1H and alpha1G in the sperm of varicocele patients and their implication]. Zhonghua Nan Ke Xue. 2012;18:331-4 pubmed
  68. Park H, Park S, Ahn E, Lee S, Seo H, Lee J. Asp residues of the Glu-Glu-Asp-Asp pore filter contribute to ion permeation and selectivity of the Ca(v)3.2 T-type channel. Cell Calcium. 2013;54:226-35 pubmed publisher
    ..2, including relative permeability between Ba2+ and Ca2+, anomalous mole fraction effect (AMFE), voltage dependency of channel activation, Cd2+ blocking sensitivity, and pH effects, in distinctive ways. ..
  69. Chemin J, Taiakina V, Monteil A, Piazza M, Guan W, Stephens R, et al. Calmodulin regulates Cav3 T-type channels at their gating brake. J Biol Chem. 2017;292:20010-20031 pubmed publisher
    ..Our findings may have implications for arrhythmia disorders arising from mutations in the gating brake or CaM. ..
  70. Thuesen A, Andersen K, Lyngsø K, Burton M, Brasch Andersen C, Vanhoutte P, et al. Deletion of T-type calcium channels Cav3.1 or Cav3.2 attenuates endothelial dysfunction in aging mice. Pflugers Arch. 2018;470:355-365 pubmed publisher
    ..Changes in NO levels are involved in this phenomenon in WT and Cav3.1-/- mice. These findings suggest that T-type channels play an important role in age-induced endothelial dysfunction. ..
  71. Chen J, Zheng D, Cui H, Liu S, Zhang L, Liu C. Roles and mechanisms of TRPC3 and the PLC?/PKC/CPI-17 signaling pathway in regulating parturition. Mol Med Rep. 2017;: pubmed publisher
    ..2, Cav3.1 and Cav3.2 expression were lower in the LPS siTRPC3 group when compared with that of the LPS?treated untransfected control group...
  72. Asaga S, Ueda M, Jinno H, Kikuchi K, Itano O, Ikeda T, et al. Identification of a new breast cancer-related gene by restriction landmark genomic scanning. Anticancer Res. 2006;26:35-42 pubmed
    ..search analysis showed that these spots represented the voltage-dependent calcium channel alpha1H subunit gene (CACNA1H gene) and a locus immediately downstream of the growth factor receptor-binding protein 7 (GRB7) gene...
  73. Splawski I, Yoo D, Stotz S, Cherry A, Clapham D, Keating M. CACNA1H mutations in autism spectrum disorders. J Biol Chem. 2006;281:22085-91 pubmed
    ..Here, we identify missense mutations in the calcium channel gene CACNA1H (T-type Ca(V)3.2) in 6 of 461 individuals with ASD...
  74. Vitko I, Bidaud I, Arias J, Mezghrani A, Lory P, Perez Reyes E. The I-II loop controls plasma membrane expression and gating of Ca(v)3.2 T-type Ca2+ channels: a paradigm for childhood absence epilepsy mutations. J Neurosci. 2007;27:322-30 pubmed
    ..Single nucleotide polymorphisms in one of the T-channel genes (CACNA1H, which encodes Ca(v)3.2) are associated with childhood absence epilepsy in a Chinese population...
  75. Weiss N, Hameed S, Fernández Fernández J, Fablet K, Karmazinova M, Poillot C, et al. A Ca(v)3.2/syntaxin-1A signaling complex controls T-type channel activity and low-threshold exocytosis. J Biol Chem. 2012;287:2810-8 pubmed publisher
  76. Demers Giroux P, Bourdin B, Sauve R, Parent L. Cooperative activation of the T-type CaV3.2 channel: interaction between Domains II and III. J Biol Chem. 2013;288:29281-93 pubmed publisher
    ..Altogether, our results demonstrate that the S4-S5 and S6 helices from adjacent domains are energetically coupled during the activation of a low voltage-gated T-type CaV3 channel. ..
  77. Blesneac I, Chemin J, Bidaud I, Huc Brandt S, Vandermoere F, Lory P. Phosphorylation of the Cav3.2 T-type calcium channel directly regulates its gating properties. Proc Natl Acad Sci U S A. 2015;112:13705-10 pubmed publisher
    ..Our data show that Cav3.2 channels are highly phosphorylated in the mammalian brain and establish phosphorylation as an important mechanism involved in the dynamic regulation of Cav3.2 channel gating properties. ..
  78. Scholl U. Unanswered Questions in the Genetic Basis of Primary Aldosteronism. Horm Metab Res. 2017;: pubmed publisher
    ..of three novel hyperaldosteronism syndromes with germline variants in the KCNJ5, CACNA1D, and CACNA1H genes...
  79. Wolfe J, Wang H, Howard J, Garrison J, Barrett P. T-type calcium channel regulation by specific G-protein betagamma subunits. Nature. 2003;424:209-13 pubmed
    ..These studies identify the alpha1H channel as a new effector for G-protein betagamma subunits, and highlight the selective signalling roles available for particular betagamma combinations. ..
  80. Khosravani H, Altier C, Simms B, Hamming K, Snutch T, Mezeyova J, et al. Gating effects of mutations in the Cav3.2 T-type calcium channel associated with childhood absence epilepsy. J Biol Chem. 2004;279:9681-4 pubmed
    ..Chan, P., Shen, Y., and Wu, X. (2003) Ann. Neurol. 54, 239-243) 12 missense mutations were identified in the CACNA1H (Ca(v)3.2) gene in 14 of 118 patients with CAE but not in 230 control individuals...
  81. Sun H, Varela D, Chartier D, Ruben P, Nattel S, Zamponi G, et al. Differential interactions of Na+ channel toxins with T-type Ca2+ channels. J Gen Physiol. 2008;132:101-13 pubmed publisher
  82. Perez Reyes E. Characterization of the gating brake in the I-II loop of CaV3 T-type calcium channels. Channels (Austin). 2010;4:453-8 pubmed
  83. Hansen P, Poulsen C, Walter S, Marcussen N, Cribbs L, Skøtt O, et al. Functional importance of L- and P/Q-type voltage-gated calcium channels in human renal vasculature. Hypertension. 2011;58:464-70 pubmed publisher
  84. Boycott H, Dallas M, Elíes J, Pettinger L, Boyle J, Scragg J, et al. Carbon monoxide inhibition of Cav3.2 T-type Ca2+ channels reveals tonic modulation by thioredoxin. FASEB J. 2013;27:3395-407 pubmed publisher
    ..CO modulation of T-type channels has widespread implications for diverse physiological and pathophysiological mechanisms, such as excitability, contractility, and proliferation...
  85. Gadotti V, Caballero A, Berger N, Gladding C, Chen L, Pfeifer T, et al. Small organic molecule disruptors of Cav3.2 - USP5 interactions reverse inflammatory and neuropathic pain. Mol Pain. 2015;11:12 pubmed publisher
    ..Overall, our findings provide proof of concept for a new class of analgesics that target T-type channel deubiquitination. ..
  86. Lin S, Wang B, Zhang F, Fei Y, Gu J, Li J, et al. T-type calcium channels, but not Cav3.2, in the peripheral sensory afferents are involved in acute itch in mice. Biochem Biophys Res Commun. 2017;487:801-806 pubmed publisher
    ..1 or Cav3.3, but not Cav3.2 channel, have an important role in acute itch processing, and their distinctive roles in modulating acute itch are worthy of further investigation. ..
  87. Sankhe S, Manousakidi S, Antigny F, Arthur Ataam J, Bentebbal S, Ruchon Y, et al. T-type Ca2+ channels elicit pro-proliferative and anti-apoptotic responses through impaired PP2A/Akt1 signaling in PASMCs from patients with pulmonary arterial hypertension. Biochim Biophys Acta Mol Cell Res. 2017;1864:1631-1641 pubmed publisher
  88. Jagannathan S, Punt E, Gu Y, Arnoult C, Sakkas D, Barratt C, et al. Identification and localization of T-type voltage-operated calcium channel subunits in human male germ cells. Expression of multiple isoforms. J Biol Chem. 2002;277:8449-56 pubmed
    ..We conclude that low voltage activated voltage-operated Ca(2+) channels are expressed in cells of the human male germ line. ..
  89. Chen Y, Lu J, Pan H, Zhang Y, Wu H, Xu K, et al. Association between genetic variation of CACNA1H and childhood absence epilepsy. Ann Neurol. 2003;54:239-43 pubmed
    Direct sequencing of exons 3 to 35 and the exon-intron boundaries of the CACNA1H gene was conducted in 118 childhood absence epilepsy patients of Han ethnicity recruited from North China...
  90. Chioza B, Everett K, Aschauer H, Brouwer O, Callenbach P, Covanis A, et al. Evaluation of CACNA1H in European patients with childhood absence epilepsy. Epilepsy Res. 2006;69:177-81 pubmed
    b>CACNA1H was evaluated in a resource of Caucasian European patients with childhood absence epilepsy by linkage analysis and typing of sequence variants previously identified in Chinese patients...
  91. David L, Garcia E, Cain S, Thau E, Tyson J, Snutch T. Splice-variant changes of the Ca(V)3.2 T-type calcium channel mediate voltage-dependent facilitation and associate with cardiac hypertrophy and development. Channels (Austin). 2010;4:375-89 pubmed publisher
    ..2 channels. We conclude that Ca(V)3.2 alternative splicing generates significant T-type Ca channel structural and functional diversity with potential implications relevant to cardiac developmental and pathophysiological states. ..
  92. Orestes P, Bojadzic D, Lee J, Leach E, Salajegheh R, Digruccio M, et al. Free radical signalling underlies inhibition of CaV3.2 T-type calcium channels by nitrous oxide in the pain pathway. J Physiol. 2011;589:135-48 pubmed publisher
    ..These findings reveal a novel mechanism of interaction between N2O and ion channels, furthering our understanding of this widely used analgesic in pain processing...