| Subcellular localization and ER-mediated cytotoxic function of alpha1A and alpha1ACT in spinocerebellar ataxia type 6. | Subcellular localization and ER-mediated cytotoxic function of α1A and α1ACT in spinocerebellar ataxia type 6.
Wang D, Honda S, Shin MK, Watase K, Mizusawa H, Ishikawa K, Shimizu S. | 02/8/2024 |
| 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 |
| Complex effects on CaV2.1 channel gating caused by a CACNA1A variant associated with a severe neurodevelopmental disorder. | Complex effects on Ca(V)2.1 channel gating caused by a CACNA1A variant associated with a severe neurodevelopmental disorder.
Grosso BJ, Kramer AA, Tyagi S, Bennett DF, Tifft CJ, D'Souza P, Wangler MF, Macnamara EF, Meza U, Bannister RA., Free PMC Article | 06/11/2022 |
| Reversing frontal disinhibition rescues behavioural deficits in models of CACNA1A-associated neurodevelopment disorders. | Reversing frontal disinhibition rescues behavioural deficits in models of CACNA1A-associated neurodevelopment disorders.
Lupien-Meilleur A, Jiang X, Lachance M, Taschereau-Dumouchel V, Gagnon L, Vanasse C, Lacaille JC, Rossignol E. | 03/19/2022 |
| Pavlovian eyeblink conditioning is severely impaired in tottering mice. | Pavlovian eyeblink conditioning is severely impaired in tottering mice.
de Oude NL, Hoebeek FE, Ten Brinke MM, de Zeeuw CI, Boele HJ. | 10/30/2021 |
| Failed Neuroprotection of Combined Inhibition of L-Type and ASIC1a Calcium Channels with Nimodipine and Amiloride. | Failed Neuroprotection of Combined Inhibition of L-Type and ASIC1a Calcium Channels with Nimodipine and Amiloride.
Ort J, Kremer B, Grüßer L, Blaumeiser-Debarry R, Clusmann H, Coburn M, Höllig A, Lindauer U., Free PMC Article | 03/6/2021 |
| Adult loss of Cacna1a in mice recapitulates childhood absence epilepsy by distinct thalamic bursting mechanisms. | Adult loss of Cacna1a in mice recapitulates childhood absence epilepsy by distinct thalamic bursting mechanisms.
Miao QL, Herlitze S, Mark MD, Noebels JL., Free PMC Article | 08/22/2020 |
| Co-immunoprecipitations from brain tissue is consistent with the formation of a protein complex between RB-3alpha and RB-3beta and both Cav2.2 and the related Cav2.1 calcium channel. | Interactions of Rabconnectin-3 with Cav2 calcium channels.
Gandini MA, Souza IA, Fan J, Li K, Wang D, Zamponi GW., Free PMC Article | 06/6/2020 |
| These novel findings have important implications for understanding the role of AnkB and Cav2.1 in the regulation of neuronal function in health and disease. | Ankyrin B and Ankyrin B variants differentially modulate intracellular and surface Cav2.1 levels.
Choi CSW, Souza IA, Sanchez-Arias JC, Zamponi GW, Arbour LT, Swayne LA., Free PMC Article | 06/6/2020 |
| Facilitation of calcium entry through CaV2.1 channels makes surprisingly little contribution to synaptic facilitation under physiological conditions. Instead, CaV2.1 facilitation offsets CaV2.1 inactivation to produce remarkably stable calcium influx during high-frequency activation. | The Role of Ca(V)2.1 Channel Facilitation in Synaptic Facilitation.
Weyrer C, Turecek J, Niday Z, Liu PW, Nanou E, Catterall WA, Bean BP, Regehr WG., Free PMC Article | 04/18/2020 |
| 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. Perinatal loss of alpha1ACT leads to motor dysfunction through disruption of neurogenesis and synaptic regulatory networks. However, its elimination in adulthood has minimal effect on the cerebellum. | 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 |
| These data identify distinct roles for CAST/ELKS as positive regulators of CaV2.1 channel density. | CAST/ELKS Proteins Control Voltage-Gated Ca(2+) Channel Density and Synaptic Release Probability at a Mammalian Central Synapse.
Dong W, Radulovic T, Goral RO, Thomas C, Suarez Montesinos M, Guerrero-Given D, Hagiwara A, Putzke T, Hida Y, Abe M, Sakimura K, Kamasawa N, Ohtsuka T, Young SM Jr., Free PMC Article | 11/9/2019 |
| A homozygous Cacna1a animal model identified discriminative features of fatal seizures compared to non-fatal seizures. | Brainstem spreading depolarization and cortical dynamics during fatal seizures in Cacna1a S218L mice.
Loonen ICM, Jansen NA, Cain SM, Schenke M, Voskuyl RA, Yung AC, Bohnet B, Kozlowski P, Thijs RD, Ferrari MD, Snutch TP, van den Maagdenberg AMJM, Tolner EA., Free PMC Article | 09/21/2019 |
| The results propose that CaV2.1 levels in the mammalian active zones are not saturated and that synaptic strength can be modulated by increasing CaV2.1 levels to regulate neuronal circuit output. | Ca(V)2.1 α(1) Subunit Expression Regulates Presynaptic Ca(V)2.1 Abundance and Synaptic Strength at a Central Synapse.
Lübbert M, Goral RO, Keine C, Thomas C, Guerrero-Given D, Putzke T, Satterfield R, Kamasawa N, Young SM Jr., Free PMC Article | 08/17/2019 |
| Munc13-3 regulates the density of Cav2.1 and Cav2.2 channels, alters the localization of Cav2.1, and is required for the development of tight, nanodomain coupling at parallel-fiber active zones. | Munc13-3 Is Required for the Developmental Localization of Ca(2+) Channels to Active Zones and the Nanopositioning of Ca(v)2.1 Near Release Sensors.
Kusch V, Bornschein G, Loreth D, Bank J, Jordan J, Baur D, Watanabe M, Kulik A, Heckmann M, Eilers J, Schmidt H. | 06/1/2019 |
| Study demonstrates that the functional defects in Cav2.1+/R1497X knock-in mice are due to the dominant-negative suppression of Cav2.1 channels and attests to the importance of the Cav2.1+/R1497X mouse model for studies of Episodic Ataxia type 2 pathophysiology as well as the development of therapeutic strategies for this disease. | Characterization of the dominant inheritance mechanism of Episodic Ataxia type 2.
Dorgans K, Salvi J, Bertaso F, Bernard L, Lory P, Doussau F, Mezghrani A. | 05/19/2018 |
| These results identified a region that directly controlled fast synaptic vesicle release and vesicle docking at the active zone independent of CaV2.1 calcium channel abundance. | A novel region in the Ca(V)2.1 α(1) subunit C-terminus regulates fast synaptic vesicle fusion and vesicle docking at the mammalian presynaptic active zone.
Lübbert M, Goral RO, Satterfield R, Putzke T, van den Maagdenberg AM, Kamasawa N, Young SM Jr., Free PMC Article | 04/14/2018 |
| These results demonstrate that a functional deficit in P/Q-type channels does not alter propulsive colonic motility. Myenteric neuron L-type Ca(2+) channel function increases to compensate for loss of functional P/Q-type Ca(2+) channels. | Upregulation of L-type calcium channels in colonic inhibitory motoneurons of P/Q-type calcium channel-deficient mice.
Rodriguez-Tapia E, Perez-Medina A, Bian X, Galligan JJ., Free PMC Article | 07/1/2017 |
| Electrophysiological characterization of VDCC currents revealed that the suppressive effect of RIM2alpha on voltage-dependent inactivation (VDI) was stronger than that of RIM1alpha for the CaV2.1 variant containing the region encoded by exons 44 and 47. | C-terminal splice variants of P/Q-type Ca(2+) channel Ca(V)2.1 α(1) subunits are differentially regulated by Rab3-interacting molecule proteins.
Hirano M, Takada Y, Wong CF, Yamaguchi K, Kotani H, Kurokawa T, Mori MX, Snutch TP, Ronjat M, De Waard M, Mori Y., Free PMC Article | 06/10/2017 |
| Cacna1a mutation plays a significant role in protein expression patterns in cerebellum of mutant mice. | Protein expression pattern in cerebellum of Cav2.1 mutant, tottering-6j mice.
Kim TY, Niimi K, Takahashi E., Free PMC Article | 03/18/2017 |
| Our findings that BAG3 is localized at the sarcolemma and t-tubules while modulating myocyte contraction and action potential duration through specific interaction with the beta1-adrenergic receptor and L-type Ca(2+) channel provide novel insight into the role of BAG3 in cardiomyopathies and increased arrhythmia risks in heart failure. | BAG3 regulates contractility and Ca(2+) homeostasis in adult mouse ventricular myocytes.
Feldman AM, Gordon J, Wang J, Song J, Zhang XQ, Myers VD, Tilley DG, Gao E, Hoffman NE, Tomar D, Madesh M, Rabinowitz J, Koch WJ, Su F, Khalili K, Cheung JY., Free PMC Article | 12/17/2016 |
| Findings demonstrate that the mutant Cav2.1 channel exerts a protective effect against cryogenic brain injury in rolling Nagoya mice | Analysis of the protective effects of a neuronal Cav2.1 calcium channel in brain injury.
Kim TY, Yoshimoto T, Aoyama Y, Niimi K, Takahashi E. | 10/1/2016 |
| regulation of CaV2.1 channels by calcium sensor proteins is required for normal short-term plasticity | Calcium sensor regulation of the CaV2.1 Ca2+ channel contributes to short-term synaptic plasticity in hippocampal neurons.
Nanou E, Sullivan JM, Scheuer T, Catterall WA., Free PMC Article | 06/28/2016 |
| results indicate that regulation of CaV2.1 channels by Ca(2+) sensor proteins is essential for normal synaptic plasticity at the neuromuscular junction and for muscle strength, endurance, and motor coordination in mice in vivo | Altered short-term synaptic plasticity and reduced muscle strength in mice with impaired regulation of presynaptic CaV2.1 Ca2+ channels.
Nanou E, Yan J, Whitehead NP, Kim MJ, Froehner SC, Scheuer T, Catterall WA., Free PMC Article | 06/28/2016 |
| 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 |