| The Transcription Factor, alpha1ACT, Acts Through a MicroRNA Network to Regulate Neurogenesis and Cell Death During Neonatal Cerebellar Development. | The Transcription Factor, α1ACT, Acts Through a MicroRNA Network to Regulate Neurogenesis and Cell Death During Neonatal Cerebellar Development.
Wei C, Benzow K, Koob MD, Gomez CM, Du X., Free PMC Article | 08/24/2023 |
| Scn1a and Cacna1a mutations mutually alter their original phenotypes in rats. | Scn1a and Cacna1a mutations mutually alter their original phenotypes in rats.
Ohmori I, Kobayashi K, Ouchida M. | 10/23/2021 |
| Response of Voltage-Gated Sodium and Calcium Channels Subtypes on Dehydroepiandrosterone Treatment in Iron-Induced Epilepsy. | Response of Voltage-Gated Sodium and Calcium Channels Subtypes on Dehydroepiandrosterone Treatment in Iron-Induced Epilepsy.
Prakash C, Mishra M, Kumar P, Kumar V, Sharma D. | 09/4/2021 |
| Ameliorative effect of curcumin on altered expression of CACNA1A and GABRD in the pathogenesis of FeCl3-induced epilepsy. | Ameliorative effect of curcumin on altered expression of CACNA1A and GABRD in the pathogenesis of FeCl(3)-induced epilepsy.
Kumar P, Sharma D. | 06/26/2021 |
| Protein Kinase CK2 Controls CaV2.1-Dependent Calcium Currents and Insulin Release in Pancreatic beta-Cells. | Protein Kinase CK2 Controls Ca(V)2.1-Dependent Calcium Currents and Insulin Release in Pancreatic β-Cells.
Scheuer R, Philipp SE, Becker A, Nalbach L, Ampofo E, Montenarh M, Götz C., Free PMC Article | 02/27/2021 |
| alpha1ACT, as a transcription factor and secondary protein of CACNA1A mRNA, drives dynamic gene expression networks within cerebellar Purkinje cells and is indispensable for neonatal survival. | α1ACT Is Essential for Survival and Early Cerebellar Programming in a Critical Neonatal Window.
Du X, Wei C, Hejazi Pastor DP, Rao ER, Li Y, Grasselli G, Godfrey J, Palmenberg AC, Andrade J, Hansel C, Gomez CM., Free PMC Article | 03/28/2020 |
| exon 47-related alternative splicing of CaV2.1 channels controls synapse-specific release properties at the level of channel mobility-dependent coupling between voltage-gated calcium channels and synaptic vesicles | Transient Confinement of Ca(V)2.1 Ca(2+)-Channel Splice Variants Shapes Synaptic Short-Term Plasticity.
Heck J, Parutto P, Ciuraszkiewicz A, Bikbaev A, Freund R, Mitlöhner J, Andres-Alonso M, Fejtova A, Holcman D, Heine M. | 10/26/2019 |
| L-type Ca(2+) channels are involved in IFN-gamma-induced signaling in rat ventricular cardiomyocytes. | L-type Ca(2+) channels' involvement in IFN-γ-induced signaling in rat ventricular cardiomyocytes.
Mitrokhin V, Filatova T, Shim A, Bilichenko A, Abramochkin D, Kamkin A, Mladenov M. | 03/30/2019 |
| Conclude that expression of the Cacna1a mRNA increased before the onset of alcohol withdrawal syndrome susceptibility, suggesting that altered CaV2.1 channel expression may play a role in AWS pathogenesis. | Alcohol withdrawal upregulates mRNA encoding for Ca(V)2.1-α1 subunit in the rat inferior colliculus.
Newton J, Suman S, Akinfiresoye LR, Datta K, Lovinger DM, N'Gouemo P., Free PMC Article | 09/22/2018 |
| postulate that the N-terminus of the truncated channel plays an essential part in its interaction with the full-length CaV2.1, which prevents the correct folding of the wild-type channel | A CaV2.1 N-terminal fragment relieves the dominant-negative inhibition by an Episodic ataxia 2 mutant.
Dahimene S, Page KM, Nieto-Rostro M, Pratt WS, D'Arco M, Dolphin AC., Free PMC Article | 03/3/2018 |
| Thus, GHSR1a differentially inhibits CaV2 channels by Gi/o or Gq protein pathways depending on its mode of activation. | Constitutive and ghrelin-dependent GHSR1a activation impairs CaV2.1 and CaV2.2 currents in hypothalamic neurons.
López Soto EJ, Agosti F, Cabral A, Mustafa ER, Damonte VM, Gandini MA, Rodríguez S, Castrogiovanni D, Felix R, Perelló M, Raingo J., Free PMC Article | 05/28/2016 |
| the consensus motifs of S-nitrosylation were much more abundant in Cav2.2 than in Cav1.2 and Cav2.1. | Molecular Basis of Regulating High Voltage-Activated Calcium Channels by S-Nitrosylation.
Zhou MH, Bavencoffe A, Pan HL., Free PMC Article | 04/23/2016 |
| data suggest that the different roles that Ca(V)2.1 and Ca(V)2.2 play in MNC secretion may be a result of the different levels of expression of Ca(V)2.1 in VP and OT MNCs | Expression of CaV 2.2 and splice variants of CaV 2.1 in oxytocin- and vasopressin-releasing supraoptic neurones.
Wang D, Fisher TE. | 10/18/2014 |
| the contribution of Ca(V)2.1 to complex cognitive functions | Ablation of Ca(V)2.1 voltage-gated Ca²⁺ channels in mouse forebrain generates multiple cognitive impairments.
Mallmann RT, Elgueta C, Sleman F, Castonguay J, Wilmes T, van den Maagdenberg A, Klugbauer N., Free PMC Article | 08/9/2014 |
| By transducing presynaptic action potential firings into unique Ca(2+) signals and vesicle release profiles, Cav2.1 channels contribute to the encoding and processing of neural information | Cav2.1 channels control multivesicular release by relying on their distance from exocytotic Ca2+ sensors at rat cerebellar granule cells.
Satake S, Imoto K., Free PMC Article | 03/15/2014 |
| Calcium currents are enhanced by alpha2delta-1 lacking its membrane anchor | Calcium currents are enhanced by α2δ-1 lacking its membrane anchor.
Kadurin I, Alvarez-Laviada A, Ng SF, Walker-Gray R, D'Arco M, Fadel MG, Pratt WS, Dolphin AC., Free PMC Article | 12/22/2012 |
| Gem contains two candidate inhibitory sites, each capable of producing full inhibition of P/Q-type Ca(2+) channels. | Molecular determinants of Gem protein inhibition of P/Q-type Ca2+ channels.
Fan M, Zhang WK, Buraei Z, Yang J., Free PMC Article | 09/15/2012 |
| Lowering glucose level enhances the activity of P/Q type Ca(2+)channels and elevates [Ca(2+)](i) level in hypothalamic arcuate nucleus neurons via inhibition of GSK3beta. | Lowering glucose level elevates [Ca2+]i in hypothalamic arcuate nucleus NPY neurons through P/Q-type Ca2+ channel activation and GSK3β inhibition.
Chen Y, Zhou J, Xie N, Huang C, Zhang JQ, Hu ZL, Ni L, Jin Y, Wang F, Chen JG, Long LH., Free PMC Article | 09/1/2012 |
| Cav2.1 channels, along with dopamine D3 receptors, mediate upregulation of dopamine D2 receptors in dopamine-denervated striatum. | Upregulation of D2-class signaling in dopamine-denervated striatum is in part mediated by D3 receptors acting on Ca V 2.1 channels via PIP2 depletion.
Prieto GA, Perez-Burgos A, Palomero-Rivero M, Galarraga E, Drucker-Colin R, Bargas J. | 04/21/2012 |
| The invertebrate LCav2 channel does not exhibit any of the hallmarks of mammalian voltage-dependent G-protein inhibition. | G-proteins modulate invertebrate synaptic calcium channel (LCav2) differently from the classical voltage-dependent regulation of mammalian Cav2.1 and Cav2.2 channels.
Huang X, Senatore A, Dawson TF, Quan Q, Spafford JD. | 09/6/2010 |
| The results indicate that muscarinic M(1) modulation of Ca(V)2.1 Ca(2+) channels in these neurons involves phosphoinositide hydrolysis. | CaV2.1 channels are modulated by muscarinic M1 receptors through phosphoinositide hydrolysis in neostriatal neurons.
Perez-Burgos A, Prieto GA, Galarraga E, Bargas J. | 03/1/2010 |
| Introduction into Ca(v)2.1 of the homologous mutation of Ca(v)1.2 causing the Timothy syndrome questions the role of V421 in the phenotypic definition of P-type Ca(2+) channel. | Introduction into Ca(v)2.1 of the homologous mutation of Ca(v)1.2 causing the Timothy syndrome questions the role of V421 in the phenotypic definition of P-type Ca(2+) channel.
Cens T, Leyris JP, Charnet P. | 01/21/2010 |
| Novel splice variants of rat CaV2.1 that lack much of the synaptic protein interaction site are expressed in neuroendocrine cells. | Novel splice variants of rat CaV2.1 that lack much of the synaptic protein interaction site are expressed in neuroendocrine cells.
Rajapaksha WR, Wang D, Davies JN, Chen L, Zamponi GW, Fisher TE., Free PMC Article | 01/21/2010 |
| Data show that the Drosophila cacophony ts2 mutation reduces presynaptic Ca2+ entry and defines an important element in Cav2.1 channel inactivation | The Drosophila cacts2 mutation reduces presynaptic Ca2+ entry and defines an important element in Cav2.1 channel inactivation.
Macleod GT, Chen L, Karunanithi S, Peloquin JB, Atwood HL, McRory JE, Zamponi GW, Charlton MP. | 01/21/2010 |
| Essential in Ca++ selectivity over other divalent cations, at a conserved EEEE locus. | Molecular determinant for specific Ca/Ba selectivity profiles of low and high threshold Ca2+ channels.
Cens T, Rousset M, Kajava A, Charnet P., Free PMC Article | 01/21/2010 |