Cacna1h

Summary

Gene Symbol: Cacna1h
Description: calcium channel, voltage-dependent, T type, alpha 1H subunit
Alias: Cav3.2, MNCb-1209, alpha13.2, voltage-dependent T-type calcium channel subunit alpha-1H, T-type Cav3.2, calcium channel alpha13.2 subunit, low-voltage-activated calcium channel alpha13.2 subunit, voltage-gated calcium channel subunit alpha Cav3.2
Species: mouse
Products:     Cacna1h

Top Publications

  1. Son W, Han C, Lee J, Jung K, Lee H, Choo Y. Developmental expression patterns of alpha1H T-type Ca2+ channels during spermatogenesis and organogenesis in mice. Dev Growth Differ. 2002;44:181-90 pubmed
    ..On E15, signals were detected throughout all organs of the embryo. These findings indicate that the expression of alpha1H T-type Ca2+ channels is spatio-temporally regulated during spermatogenesis and organogenesis. ..
  2. 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...
  3. Chen W, Liu I, Chang Y, Chen Y, Chen C, Yen C, et al. Ca(v)3.2 T-type Ca2+ channel-dependent activation of ERK in paraventricular thalamus modulates acid-induced chronic muscle pain. J Neurosci. 2010;30:10360-8 pubmed publisher
    ..Our findings suggest that Ca(v)3.2 T-channel-dependent activation of ERK in PVA is required for the development of acid-induced chronic mechanical hyperalgesia. ..
  4. Chen C, Shen J, Chung N, Min M, Cheng S, Liu I. Retrieval of context-associated memory is dependent on the Ca(v)3.2 T-type calcium channel. PLoS ONE. 2012;7:e29384 pubmed publisher
    ..Taken together, our results demonstrate that retrieval of context-associated memory is dependent on the Ca(v)3.2 T-type Ca²? channel. ..
  5. Jaleel N, Nakayama H, Chen X, Kubo H, MacDonnell S, Zhang H, et al. Ca2+ influx through T- and L-type Ca2+ channels have different effects on myocyte contractility and induce unique cardiac phenotypes. Circ Res. 2008;103:1109-19 pubmed publisher
  6. Choi S, Na H, Kim J, Lee J, Lee S, Kim D, et al. Attenuated pain responses in mice lacking Ca(V)3.2 T-type channels. Genes Brain Behav. 2007;6:425-31 pubmed
    ..The present study reveals that the Ca(V)3.2 subtype of T-type Ca(2+) channels are important in the peripheral processing of noxious signals, regardless of modality, duration or affected tissue type...
  7. 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. ..
  8. Bourinet E, Alloui A, Monteil A, Barrere C, Couette B, Poirot O, et al. Silencing of the Cav3.2 T-type calcium channel gene in sensory neurons demonstrates its major role in nociception. EMBO J. 2005;24:315-24 pubmed
    ..Taken together, the results provide direct evidence linking CaV3.2 T-type channels to pain perception and suggest that CaV3.2 may offer a specific molecular target for the treatment of pain. ..
  9. García Caballero A, Gadotti V, Stemkowski P, Weiss N, Souza I, Hodgkinson V, et al. The deubiquitinating enzyme USP5 modulates neuropathic and inflammatory pain by enhancing Cav3.2 channel activity. Neuron. 2014;83:1144-58 pubmed publisher
    ..Altogether, our experiments reveal a cell signaling pathway that regulates T-type channel activity and their role in nociceptive signaling. ..

More Information

Publications78

  1. 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...
  2. Latham J, Pathirathna S, Jagodic M, Choe W, Levin M, Nelson M, et al. Selective T-type calcium channel blockade alleviates hyperalgesia in ob/ob mice. Diabetes. 2009;58:2656-65 pubmed publisher
    ..Our results indicate that pharmacological antagonism of T-channels is potentially an important novel therapeutic approach for the management of painful diabetic neuropathy. ..
  3. Chiang C, Huang C, Chieng H, Chang Y, Chang D, Chen J, et al. The Ca(v)3.2 T-type Ca(2+) channel is required for pressure overload-induced cardiac hypertrophy in mice. Circ Res. 2009;104:522-30 pubmed publisher
    ..Our results provide strong genetic evidence that Ca(v)3.2 indeed plays a pivotal role in the induction of calcineurin/NFAT hypertrophic signaling and is crucial for the activation of pathological cardiac hypertrophy. ..
  4. Markandeya Y, Phelan L, Woon M, Keefe A, Reynolds C, August B, et al. Caveolin-3 Overexpression Attenuates Cardiac Hypertrophy via Inhibition of T-type Ca2+ Current Modulated by Protein Kinase Cα in Cardiomyocytes. J Biol Chem. 2015;290:22085-100 pubmed publisher
    ..In conclusion, we show that stable Cav-3 expression is essential for protecting the signaling mechanisms in pharmacologically and pressure overload-induced cardiac hypertrophy. ..
  5. Alnawaiseh M, Albanna W, Chen C, Campbell K, Hescheler J, Lüke M, et al. Two separate Ni(2+) -sensitive voltage-gated Ca(2+) channels modulate transretinal signalling in the isolated murine retina. Acta Ophthalmol. 2011;89:e579-90 pubmed publisher
  6. Rodríguez Gómez J, Levitsky K, Lopez Barneo J. T-type Ca2+ channels in mouse embryonic stem cells: modulation during cell cycle and contribution to self-renewal. Am J Physiol Cell Physiol. 2012;302:C494-504 pubmed publisher
    ..We propose that Ca(2+) entry mediated by Ca(v)3.2 channels might be one of the intracellular signals that participate in the complex network responsible for ES cell self-renewal. ..
  7. Okubo K, Matsumura M, Kawaishi Y, Aoki Y, Matsunami M, Okawa Y, et al. Hydrogen sulfide-induced mechanical hyperalgesia and allodynia require activation of both Cav3.2 and TRPA1 channels in mice. Br J Pharmacol. 2012;166:1738-43 pubmed publisher
    ..Mechanical hyperalgesia and allodynia induced by NaHS/H(2)S required activation of both Ca(v)3.2 and TRPA1 channels in mice. ..
  8. Li Y, Wang F, Zhang X, Qi Z, Tang M, Szeto C, et al. ?-Adrenergic stimulation increases Cav3.1 activity in cardiac myocytes through protein kinase A. PLoS ONE. 2012;7:e39965 pubmed publisher
    ..1)) in cardiomyocytes(,) which is mediated by the cAMP/PKA pathway. The upregulation of I(Ca-T(3.1)) by the ?-adrenergic system could play important roles in cellular functions involving Cav3.1. ..
  9. Thuesen A, Andersen H, Cardel M, Toft A, Walter S, Marcussen N, et al. Differential effect of T-type voltage-gated Ca2+ channel disruption on renal plasma flow and glomerular filtration rate in vivo. Am J Physiol Renal Physiol. 2014;307:F445-52 pubmed publisher
    ..1 channels in vivo contribute to renal vascular resistance. It is suggested that endothelial and nerve localization of Cav3.2 and Cav3.1, respectively, may account for the observed effects. ..
  10. Zheng H, Park K, Koh S, Sanders K. Expression and function of a T-type Ca2+ conductance in interstitial cells of Cajal of the murine small intestine. Am J Physiol Cell Physiol. 2014;306:C705-13 pubmed publisher
    ..6 to 7.5 ms [temperature coefficient (Q10) = 3.0]. Molecular studies showed expression of Cacna1g (Cav3.1) and Cacna1h (Cav3.2) in ICC...
  11. Cribbs L, Martin B, Schroder E, Keller B, Delisle B, Satin J. Identification of the t-type calcium channel (Ca(v)3.1d) in developing mouse heart. Circ Res. 2001;88:403-7 pubmed
    ..We demonstrate that 100 micromol/L Ni(2+) partially blocked alpha1G currents under physiological external Ca(2+). We conclude that alpha1G T-type Ca(2+) channels are functional in midgestational fetal myocardium. ..
  12. Chung N, Huang Y, Chang C, Liao J, Yang C, Chen C, et al. Behavior training reverses asymmetry in hippocampal transcriptome of the cav3.2 knockout mice. PLoS ONE. 2015;10:e0118832 pubmed publisher
    ..To our knowledge, these results demonstrate for the first time the asymmetric effects of the Cav3.2 and its partial reversal by behavior training on the hippocampal transcriptome. ..
  13. Cui J, Ivanova E, Qi L, Pan Z. Expression of CaV3.2 T-type Ca²? channels in a subpopulation of retinal type-3 cone bipolar cells. Neuroscience. 2012;224:63-9 pubmed publisher
    ..2 Ca(2+) channels contribute to the T-type Ca(2+) current in a subpopulation of type-3 CBCs. The findings of this study provide new insights into understanding the functional roles of T-type Ca(2+) channels in retinal processing. ..
  14. 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. ..
  15. Berthier C, Monteil A, Lory P, Strube C. Alpha(1H) mRNA in single skeletal muscle fibres accounts for T-type calcium current transient expression during fetal development in mice. J Physiol. 2002;539:681-91 pubmed
  16. Le Quang K, Naud P, Qi X, Duval F, Shi Y, Gillis M, et al. Role of T-type calcium channel subunits in post-myocardial infarction remodelling probed with genetically engineered mice. Cardiovasc Res. 2011;91:420-8 pubmed publisher
    ..1 expression leads to impaired cardiac function and enhanced arrhythmia vulnerability post-MI, whereas Cav3.2 elimination has no effect. ..
  17. Berger N, Gadotti V, Petrov R, Chapman K, Diaz P, Zamponi G. NMP-7 inhibits chronic inflammatory and neuropathic pain via block of Cav3.2 T-type calcium channels and activation of CB2 receptors. Mol Pain. 2014;10:77 pubmed publisher
    ..Thus, this study provides a novel therapeutic avenue for managing chronic pain conditions via mixed CB ligands/T-type channel blockers. ..
  18. Van Loo K, Schaub C, Pernhorst K, Yaari Y, Beck H, Schoch S, et al. Transcriptional regulation of T-type calcium channel CaV3.2: bi-directionality by early growth response 1 (Egr1) and repressor element 1 (RE-1) protein-silencing transcription factor (REST). J Biol Chem. 2012;287:15489-501 pubmed publisher
    ..2 (Cacna1h). First, we determined the promoter region and observed several stimulatory and inhibitory clusters...
  19. Hamby A, Rosa J, Hsu C, Feller M. CaV3.2 KO mice have altered retinal waves but normal direction selectivity. Vis Neurosci. 2015;32:E003 pubmed publisher
  20. Bernhardt M, Zhang Y, Erxleben C, Padilla Banks E, McDonough C, Miao Y, et al. CaV3.2 T-type channels mediate Ca²⁺ entry during oocyte maturation and following fertilization. J Cell Sci. 2015;128:4442-52 pubmed publisher
    ..Here, we tested whether the α1 subunit of the T-type channel CaV3.2, encoded by Cacna1h, mediates Ca(2+) entry into oocytes...
  21. Lee S, Lee J, Latchoumane C, Lee B, Oh S, Saud Z, et al. Rebound burst firing in the reticular thalamus is not essential for pharmacological absence seizures in mice. Proc Natl Acad Sci U S A. 2014;111:11828-33 pubmed publisher
    ..These results call into question the role of burst firing in TRN neurons in the genesis of SWDs, calling for a rethinking of the mechanism for absence seizure induction. ..
  22. Joksovic P, Nelson M, Jevtovic Todorovic V, Patel M, Perez Reyes E, Campbell K, et al. CaV3.2 is the major molecular substrate for redox regulation of T-type Ca2+ channels in the rat and mouse thalamus. J Physiol. 2006;574:415-30 pubmed
  23. Liao Y, Tsai M, Chen C, Yen C. Involvement of the Cav3.2 T-type calcium channel in thalamic neuron discharge patterns. Mol Pain. 2011;7:43 pubmed publisher
    ..The decreased occurrence and slowing of the bursts in RT neurons might cause the increased VP bursts. These changes would be factors contributing to alternation of pain behavior in the Cav3.2 KO mice. ..
  24. Tsubota M, Ozaki T, Hayashi Y, Okawa Y, Fujimura A, Sekiguchi F, et al. Prostanoid-dependent bladder pain caused by proteinase-activated receptor-2 activation in mice: Involvement of TRPV1 and T-type Ca2+ channels. J Pharmacol Sci. 2018;136:46-49 pubmed publisher
    ..Our data suggest that luminal PAR2 stimulation in the bladder causes prostanoid-dependent referred hyperalgesia in mice, which involves the activation of TRPV1 and T-type Ca2+ channels. ..
  25. Miesenbock G, De Angelis D, Rothman J. Visualizing secretion and synaptic transmission with pH-sensitive green fluorescent proteins. Nature. 1998;394:192-5 pubmed
    ..When linked to a vesicle membrane protein, pHluorins were sorted to secretory and synaptic vesicles and reported transmission at individual synaptic boutons, as well as secretion and fusion pore 'flicker' of single secretory granules. ..
  26. Porter G, Makuck R, Rivkees S. Intracellular calcium plays an essential role in cardiac development. Dev Dyn. 2003;227:280-90 pubmed
    ..These data demonstrate that proper intracellular calcium signaling is essential for normal cardiac looping, gene expression, and organ development. ..
  27. Huang Z, Lujan R, Kadurin I, Uebele V, Renger J, Dolphin A, et al. Presynaptic HCN1 channels regulate Cav3.2 activity and neurotransmission at select cortical synapses. Nat Neurosci. 2011;14:478-86 pubmed publisher
    ..2 subunit. This represents a previously unknown mechanism by which HCN channels regulate synaptic strength and thereby neural information processing and network excitability. ..
  28. Tyser R, Miranda A, Chen C, Davidson S, Srinivas S, Riley P. Calcium handling precedes cardiac differentiation to initiate the first heartbeat. elife. 2016;5: pubmed publisher
    ..NCX1 blockade impacted on CaMKII signalling to down-regulate cardiac gene expression, leading to impaired differentiation and failed crescent maturation. ..
  29. Rose K, Lunardi N, Boscolo A, Dong X, Erisir A, Jevtovic Todorovic V, et al. Immunohistological demonstration of CaV3.2 T-type voltage-gated calcium channel expression in soma of dorsal root ganglion neurons and peripheral axons of rat and mouse. Neuroscience. 2013;250:263-74 pubmed publisher
    ..The CaV3.2 expression within the soma and peripheral axons of nociceptive sensory neurons further demonstrates the importance of this channel in peripheral pain transmission. ..
  30. Tsubota Matsunami M, Noguchi Y, Okawa Y, Sekiguchi F, Kawabata A. Colonic hydrogen sulfide-induced visceral pain and referred hyperalgesia involve activation of both Ca(v)3.2 and TRPA1 channels in mice. J Pharmacol Sci. 2012;119:293-6 pubmed
    ..These findings demonstrate that H(2)S-induced colonic pain and referred hyperalgesia require activation of both Ca(v)3.2 and TRPA1 channels in mice...
  31. Gibbons S, Strege P, Lei S, Roeder J, Mazzone A, Ou Y, et al. The alpha1H Ca2+ channel subunit is expressed in mouse jejunal interstitial cells of Cajal and myocytes. J Cell Mol Med. 2009;13:4422-31 pubmed publisher
    ..Gene targeted knockout of both alleles of the cacna1h gene, which encodes the alpha(1H) Ca(2+) channel subunit, resulted in embryonic lethality because of death of the ..
  32. Lee W, Orestes P, Latham J, Naik A, Nelson M, Vitko I, et al. Molecular mechanisms of lipoic acid modulation of T-type calcium channels in pain pathway. J Neurosci. 2009;29:9500-9 pubmed publisher
    ..This study provides the first mechanistic demonstration of a nociceptive ion channel modulation that may contribute to the documented analgesic properties of lipoic acid in vivo. ..
  33. Lin S, Yu X, Wang B, Zhang Y, Sun Y, Liu X. Colocalization of insulin-like growth factor-1 receptor and T type Cav3.2 channel in dorsal root ganglia in chronic inflammatory pain mouse model. Neuroreport. 2016;27:737-43 pubmed publisher
    ..Our findings provided morphological evidence that T-type Cav3.2 channel, at least partially, mediates the pain facilitation of IGF-1/IGF-1R signaling in chronic inflammatory pain condition. ..
  34. Mikkelsen M, Björling K, Jensen L. Age-dependent impact of CaV 3.2 T-type calcium channel deletion on myogenic tone and flow-mediated vasodilatation in small arteries. J Physiol. 2016;594:5881-5898 pubmed publisher
    ..2 channels, by modulating pressure- and flow-mediated vasomotor responses to prevent excess arterial tone, protect against cardiovascular disease. ..
  35. Lin S, Tzeng B, Lee K, Smith R, Campbell K, Chen C. Cav3.2 T-type calcium channel is required for the NFAT-dependent Sox9 expression in tracheal cartilage. Proc Natl Acad Sci U S A. 2014;111:E1990-8 pubmed publisher
    ..Our findings define a previously unidentified mechanism that Ca(2+) influx via the Cav3.2 T-type Ca(2+) channel regulates Sox9 expression through the calcineurin/NFAT signaling pathway during tracheal chondrogenesis. ..
  36. Wang R, Lewin G. The Cav3.2 T-type calcium channel regulates temporal coding in mouse mechanoreceptors. J Physiol. 2011;589:2229-43 pubmed publisher
    ..The T-type calcium channel Cav3.2 is thus not only a highly specific marker of D-hair receptors but is also required to maintain their high sensitivity and above all to ensure ultra rapid temporal detection of skin movement. ..
  37. Srinivasan P, Parajuli A, Price C, Wang L, Duncan R, Kirn Safran C. Inhibition of T-Type Voltage Sensitive Calcium Channel Reduces Load-Induced OA in Mice and Suppresses the Catabolic Effect of Bone Mechanical Stress on Chondrocytes. PLoS ONE. 2015;10:e0127290 pubmed publisher
    ..Further, these findings suggest that local inhibition of T-VSCC may serve as a therapy for blocking load-induced bone formation that results in cartilage degeneration. ..
  38. Bodrikov V, Sytnyk V, Leshchyns ka I, den Hertog J, Schachner M. NCAM induces CaMKIIalpha-mediated RPTPalpha phosphorylation to enhance its catalytic activity and neurite outgrowth. J Cell Biol. 2008;182:1185-200 pubmed publisher
    ..Thus, we reveal a novel function for a cell adhesion molecule in coordination of cell behavior with intracellular phosphatase activity. ..
  39. 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...
  40. Thompson W, Majid A, Czymmek K, Ruff A, Garcia J, Duncan R, et al. Association of the ?(2)?(1) subunit with Ca(v)3.2 enhances membrane expression and regulates mechanically induced ATP release in MLO-Y4 osteocytes. J Bone Miner Res. 2011;26:2125-39 pubmed publisher
    ..2 (?(1H)) at the plasma membrane, suggesting that the diminished ATP release and ERK1/2 activation in response to membrane stretch resulted from a lack of Ca(v) 3.2 (?(1H)) at the cell membrane...
  41. Niwa N, Yasui K, Opthof T, Takemura H, Shimizu A, Horiba M, et al. Cav3.2 subunit underlies the functional T-type Ca2+ channel in murine hearts during the embryonic period. Am J Physiol Heart Circ Physiol. 2004;286:H2257-63 pubmed
    ..2 mRNA. These results indicate that Ca(v)3.2 underlies the functional T-type Ca2+ channels in the embryonic murine heart, and there is a subtype switching of transcripts from Ca(v)3.2 to Ca(v)3.1 in the perinatal period. ..
  42. Shao Y, Alicknavitch M, Farach Carson M. Expression of voltage sensitive calcium channel (VSCC) L-type Cav1.2 (alpha1C) and T-type Cav3.2 (alpha1H) subunits during mouse bone development. Dev Dyn. 2005;234:54-62 pubmed
    ..We conclude that both L-type Ca(v)1.2 (alpha(1C)) and T-type Ca(v)3.2 (alpha(1H)) VSCCs are dynamically regulated in bones and cartilages during endochondral bone development. ..
  43. Graef J, Nordskog B, Wiggins W, Godwin D. An acquired channelopathy involving thalamic T-type Ca2+ channels after status epilepticus. J Neurosci. 2009;29:4430-41 pubmed publisher
    ..We conclude that SE produces an acquired channelopathy by inducing long-term alterations in thalamic T-type channels that contribute to characteristic changes in excitability observed during epileptogenesis and SRS. ..
  44. 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. ..
  45. Mashimo T, Erven A, Spiden S, Guenet J, Steel K. Two quantitative trait loci affecting progressive hearing loss in 101/H mice. Mamm Genome. 2006;17:841-50 pubmed
    ..Finally, we found some evidence of epistatic interaction between Phl1 and Phl2. ..
  46. Dubreuil A, Boukhaddaoui H, Desmadryl G, Martinez Salgado C, Moshourab R, Lewin G, et al. Role of T-type calcium current in identified D-hair mechanoreceptor neurons studied in vitro. J Neurosci. 2004;24:8480-4 pubmed
    ..Indeed, the properties of the T-type amplifier are particularly well suited to explain the high sensitivity of D-hair mechanoreceptors to slowly moving stimuli. ..
  47. Lin S, Yu X, Liu X, Wang B, Li C, Sun Y, et al. Expression patterns of T-type Cav3.2 channel and insulin-like growth factor-1 receptor in dorsal root ganglion neurons of mice after sciatic nerve axotomy. Neuroreport. 2016;27:1174-81 pubmed publisher
    ..2 and IGF-1R expression in lumbar DRGs post-sciatic nerve axotomy and provided an insight for understanding the functions of peripheral afferent Cav3.2 channel and IGF-1/IGF-1R signaling in chronic neuropathic pain. ..
  48. Markandeya Y, Fahey J, Pluteanu F, Cribbs L, Balijepalli R. Caveolin-3 regulates protein kinase A modulation of the Ca(V)3.2 (alpha1H) T-type Ca2+ channels. J Biol Chem. 2011;286:2433-44 pubmed publisher
    ..Our findings on functional modulation of the Ca(v)3.2 channels by Cav-3 is important for understanding the compartmentalized regulation of Ca(2+) signaling during normal and pathological processes. ..
  49. Shin J, Martinez Salgado C, Heppenstall P, Lewin G. A T-type calcium channel required for normal function of a mammalian mechanoreceptor. Nat Neurosci. 2003;6:724-30 pubmed
    ..This is the first evidence that a calcium channel is required for normal function of a vertebrate mechanoreceptor. ..
  50. 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. ..
  51. Jacus M, Uebele V, Renger J, Todorovic S. Presynaptic Cav3.2 channels regulate excitatory neurotransmission in nociceptive dorsal horn neurons. J Neurosci. 2012;32:9374-82 pubmed publisher
    ..These studies provide previously unknown information regarding the role of presynaptic T-channels in nociceptive signaling in the spinal cord. ..
  52. Cazade M, Bidaud I, Hansen P, Lory P, Chemin J. 5,6-EET potently inhibits T-type calcium channels: implication in the regulation of the vascular tone. Pflugers Arch. 2014;466:1759-68 pubmed publisher
    ..2 knockout mice. Overall, our results indicate that inhibition of Cav3 currents by 5,6-EET is an important mechanism controlling the vascular tone. ..
  53. Xu M, Welling A, Paparisto S, Hofmann F, Klugbauer N. Enhanced expression of L-type Cav1.3 calcium channels in murine embryonic hearts from Cav1.2-deficient mice. J Biol Chem. 2003;278:40837-41 pubmed
    ..2 (-/-) cardiomyocytes. In summary, our results imply that calcium channel expression is dynamically regulated during heart development and that the Cav1.3 channel may substitute for Cav1.2 during early embryogenesis. ..
  54. Curran J, Musa H, Kline C, Makara M, Little S, Higgins J, et al. Eps15 Homology Domain-containing Protein 3 Regulates Cardiac T-type Ca2+ Channel Targeting and Function in the Atria. J Biol Chem. 2015;290:12210-21 pubmed publisher
  55. Becker A, Pitsch J, Sochivko D, Opitz T, Staniek M, Chen C, et al. Transcriptional upregulation of Cav3.2 mediates epileptogenesis in the pilocarpine model of epilepsy. J Neurosci. 2008;28:13341-53 pubmed publisher
    ..In addition, the appearance of spontaneous seizures was dramatically reduced in these mice. Together, these data establish transcriptional induction of Ca(v)3.2 as a critical step in epileptogenesis and neuronal vulnerability. ..
  56. Figueroa X, Chen C, Campbell K, Damon D, Day K, Ramos S, et al. Are voltage-dependent ion channels involved in the endothelial cell control of vasomotor tone?. Am J Physiol Heart Circ Physiol. 2007;293:H1371-83 pubmed
    ..2 channels. The resultant Ca(2+) influx activates endothelial nitric oxide synthase and Ca(2+)-activated K(+) channels, triggering vasodilation. ..
  57. Tzeng B, Chen Y, Huang C, Lin S, Lee K, Chen C. The Ca(v)3.1 T-type calcium channel is required for neointimal formation in response to vascular injury in mice. Cardiovasc Res. 2012;96:533-42 pubmed publisher
    ..Ca(v)3.1 is required for VSMC proliferation during neointimal formation, and blocking of Ca(v)3.1 may be beneficial for preventing restenosis. ..
  58. Makarenko V, Peng Y, Yuan G, Fox A, Kumar G, Nanduri J, et al. CaV3.2 T-type Ca²⁺ channels in H₂S-mediated hypoxic response of the carotid body. Am J Physiol Cell Physiol. 2015;308:C146-54 pubmed publisher
    ..Similar results were obtained in the carotid body and glomus cells from CaV3.2 knockout (Cacna1h(-/-)) mice...
  59. Howitt L, Kuo I, Ellis A, Chaston D, Shin H, Hansen P, et al. Chronic deficit in nitric oxide elicits oxidative stress and augments T-type calcium-channel contribution to vascular tone of rodent arteries and arterioles. Cardiovasc Res. 2013;98:449-57 pubmed publisher
    ..Our data provide evidence for a novel causal link between nitric oxide deficit, oxidative stress, and T-type calcium channel function. ..
  60. François A, Schüetter N, Laffray S, Sanguesa J, Pizzoccaro A, Dubel S, et al. The Low-Threshold Calcium Channel Cav3.2 Determines Low-Threshold Mechanoreceptor Function. Cell Rep. 2015;: pubmed publisher
    ..Collectively, our findings support a fundamental role for Cav3.2 in touch/pain pathophysiology, validating their critic pharmacological relevance to relieve mechanical and cold allodynia. ..
  61. Matsunami M, Miki T, Nishiura K, Hayashi Y, Okawa Y, Nishikawa H, et al. Involvement of the endogenous hydrogen sulfide/Ca(v) 3.2 T-type Ca2+ channel pathway in cystitis-related bladder pain in mice. Br J Pharmacol. 2012;167:917-28 pubmed publisher
    ..2 T-type Ca(2+) channels. Here, we assessed the involvement of the CSE/H(2) S/Ca(v) 3.2 pathway in cystitis-related bladder pain...
  62. Dey D, Shepherd A, Pachuau J, Martin Caraballo M. Leukemia inhibitory factor regulates trafficking of T-type Ca2+ channels. Am J Physiol Cell Physiol. 2011;300:C576-87 pubmed publisher
    ..Both P6 and U0126 also inhibited the stimulatory effect of LIF on T-type Ca(2+) channel expression. These findings demonstrate that cytokines like LIF promote the trafficking of T-type Ca(2+) channels. ..
  63. Rzhepetskyy Y, Lazniewska J, Blesneac I, Pamphlett R, Weiss N. CACNA1H missense mutations associated with amyotrophic lateral sclerosis alter Cav3.2 T-type calcium channel activity and reticular thalamic neuron firing. Channels (Austin). 2016;10:466-77 pubmed publisher
    ..2 T-type calcium channel gene (CACNA1H), in a family with an affected proband (early onset, long duration ALS) and 2 unaffected parents...
  64. Lei D, Gao X, Perez P, Ohlemiller K, Chen C, Campbell K, et al. Anti-epileptic drugs delay age-related loss of spiral ganglion neurons via T-type calcium channel. Hear Res. 2011;278:106-12 pubmed publisher
    ..To our knowledge, this is the first report of drugs capable of diminishing age-related loss of spiral ganglion neurons. ..
  65. 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. ..
  66. Kerckhove N, Mallet C, Francois A, Boudes M, Chemin J, Voets T, et al. Ca(v)3.2 calcium channels: the key protagonist in the supraspinal effect of paracetamol. Pain. 2014;155:764-72 pubmed publisher
    ..2 channel; and (3) suggests supraspinal Ca(v)3.2 inhibition as a potential pharmacological strategy to alleviate pain. ..
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