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    Cacna1b calcium channel, voltage-dependent, N type, alpha 1B subunit [ Mus musculus (house mouse) ]

    Gene ID: 12287, updated on 27-Nov-2024

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    Interleukin-1alpha links peripheral CaV2.2 channel activation to rapid adaptive increases in heat sensitivity in skin.

    Interleukin-1α links peripheral Ca(V)2.2 channel activation to rapid adaptive increases in heat sensitivity in skin.
    Salib AN, Crane MJ, Lee SH, Wainger BJ, Jamieson AM, Lipscombe D., Free PMC Article

    05/22/2024
    Cav2.2 Channels Sustain Vesicle Recruitment at a Mature Glutamatergic Synapse.

    Ca(v)2.2 Channels Sustain Vesicle Recruitment at a Mature Glutamatergic Synapse.
    Wender M, Bornschein G, Brachtendorf S, Hallermann S, Eilers J, Schmidt H., Free PMC Article

    06/12/2023
    N-type calcium channel v2.2 is a target of TCF21 in adrenocortical carcinomas.

    N-type calcium channel v2.2 is a target of TCF21 in adrenocortical carcinomas.
    Passaia BDS, Kremer JL, Fragoso MCV, Lotfi CFP.

    08/20/2022
    Constitutive activity of dopamine receptor type 1 (D1R) increases CaV2.2 currents in PFC neurons.

    Constitutive activity of dopamine receptor type 1 (D1R) increases CaV2.2 currents in PFC neurons.
    McCarthy CI, Chou-Freed C, Rodríguez SS, Yaneff A, Davio C, Raingo J., Free PMC Article

    06/12/2021
    Knockdown of microglial Cav2.2 N-type voltage-dependent Ca(2+) channel ameliorates behavioral deficits in a mouse model of Parkinson's disease.

    Knockdown of microglial Cav2.2 N-type voltage-dependent Ca(2+) channel ameliorates behavioral deficits in a mouse model of Parkinson's disease.
    Saegusa H, Li X, Wang X, Kayakiri M, Tanabe T.

    05/15/2021
    Involvement of N-type Ca(2+) channel in microglial activation and its implications to aging-induced exaggerated cytokine response.

    Involvement of N-type Ca(2+) channel in microglial activation and its implications to aging-induced exaggerated cytokine response.
    Huntula S, Saegusa H, Wang X, Zong S, Tanabe T.

    09/12/2020
    alternative splicing of Cacna1b e37a influences excitatory transmitter release and couples to complex behaviors.

    Cacna1b alternative splicing impacts excitatory neurotransmission and is linked to behavioral responses to aversive stimuli.
    Bunda A, LaCarubba B, Bertolino M, Akiki M, Bath K, Lopez-Soto J, Lipscombe D, Andrade A., Free PMC Article

    06/13/2020
    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
    The studies and identified +e18a-Cacna1b mRNA in deep cerebellar cells and spinal cord motor neurons and +e18a-Cacna1b is enriched in cholecystokinin-expressing interneurons.

    Tissue- and cell-specific expression of a splice variant in the II-III cytoplasmic loop of Cacna1b.
    Bunda A, LaCarubba B, Akiki M, Andrade A., Free PMC Article

    05/2/2020
    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
    It is essential for presynaptic neurotransmitter release.

    N-type Ca(2+) channels are affected by full-length mutant huntingtin expression in a mouse model of Huntington's disease.
    Silva FR, Miranda AS, Santos RPM, Olmo IG, Zamponi GW, Dobransky T, Cruz JS, Vieira LB, Ribeiro FM.

    12/2/2017
    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
    Blockade of Cav2.2 in inflammatory arthritis leads to up-regulation of the osteoclast activator RANKL and concomitant joint and bone destruction.

    Suppression of Peripheral Pain by Blockade of Voltage-Gated Calcium 2.2 Channels in Nociceptors Induces RANKL and Impairs Recovery From Inflammatory Arthritis in a Mouse Model.
    Baddack U, Frahm S, Antolin-Fontes B, Grobe J, Lipp M, Müller G, Ibañez-Tallon I., Free PMC Article

    08/8/2015
    Results identified altered synaptic transmission in the olfactory system of Cav2.2-deficient mice and suggest that the olfactory system could become an attractive model to learn more about this channel and the consequences of its removal

    Altered synaptic transmission at olfactory and vomeronasal nerve terminals in mice lacking N-type calcium channel Cav2.2.
    Weiss J, Pyrski M, Weissgerber P, Zufall F.

    07/25/2015
    Both pharmacological blockade of N-type calcium channels and their genetic titration improved cardiac autonomic balance and prevented lethal arrhythmias in a mouse model of dilated cardiomyopathy and sudden arrhythmic death.

    Inhibition of N-type Ca2+ channels ameliorates an imbalance in cardiac autonomic nerve activity and prevents lethal arrhythmias in mice with heart failure.
    Yamada Y, Kinoshita H, Kuwahara K, Nakagawa Y, Kuwabara Y, Minami T, Yamada C, Shibata J, Nakao K, Cho K, Arai Y, Yasuno S, Nishikimi T, Ueshima K, Kamakura S, Nishida M, Kiyonaka S, Mori Y, Kimura T, Kangawa K, Nakao K.

    06/20/2015
    Gaba B receptors were found to mediate Cav2.2 channel inhibition.

    Novel mechanism of voltage-gated N-type (Cav2.2) calcium channel inhibition revealed through α-conotoxin Vc1.1 activation of the GABA(B) receptor.
    Huynh TG, Cuny H, Slesinger PA, Adams DJ.

    04/4/2015
    Cav2.1-2.3 have unique contributions to the dynamics at the Schaffer collateral synapse that are engaged by the complex patterns of afferent activity seen in vivo

    Distinct roles for Cav2.1-2.3 in activity-dependent synaptic dynamics.
    Ricoy UM, Frerking ME., Free PMC Article

    01/31/2015
    Results demonstrate that sensory neurons from Nf1+/- mice, exhibit increased N-type (Cav2.2) ICa and likely account for the increased release of substance P and calcitonin gene-related peptide that occurs in Nf1+/- sensory neurons

    N-type calcium current, Cav2.2, is enhanced in small-diameter sensory neurons isolated from Nf1+/- mice.
    Duan JH, Hodgdon KE, Hingtgen CM, Nicol GD., Free PMC Article

    01/17/2015
    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
    Although the mechanism of its activation is not clear at present, activation of N-type VDCC expressed in non-excitable microglial cells contributes to the pathophysiology of neuropathic pain.

    N-type voltage-dependent Ca2+ channel in non-excitable microglial cells in mice is involved in the pathophysiology of neuropathic pain.
    Saegusa H, Tanabe T.

    09/27/2014
    CaV2.2 and alpha2delta-1 are intimately associated at the plasma membrane

    Functional exofacially tagged N-type calcium channels elucidate the interaction with auxiliary α2δ-1 subunits.
    Cassidy JS, Ferron L, Kadurin I, Pratt WS, Dolphin AC., Free PMC Article

    09/13/2014
    These findings identify an interaction between ankyrin-B and both Cav2.1 and Cav2.2 at the amino acid level that is necessary for proper Cav2.1 and Cav2.2 targeting in vivo.

    Ankyrin-B regulates Cav2.1 and Cav2.2 channel expression and targeting.
    Kline CF, Scott J, Curran J, Hund TJ, Mohler PJ., Free PMC Article

    04/26/2014
    Oxidative stress-related endothelial dysfunction induced by angiotensin II is suppressed in mice lacking the N-type VDCC alpha1B subunit.

    Voltage-dependent N-type Ca2+ channels in endothelial cells contribute to oxidative stress-related endothelial dysfunction induced by angiotensin II in mice.
    Nishida M, Ishikawa T, Saiki S, Sunggip C, Aritomi S, Harada E, Kuwahara K, Hirano K, Mori Y, Kim-Mitsuyama S.

    06/29/2013
    Blocking Cav2.2 channels abolishes respiratory activity in all brainstem slices from Cav2.1 genetically ablated animals.

    Stable respiratory activity requires both P/Q-type and N-type voltage-gated calcium channels.
    Koch H, Zanella S, Elsen GE, Smith L, Doi A, Garcia AJ 3rd, Wei AD, Xun R, Kirsch S, Gomez CM, Hevner RF, Ramirez JM., Free PMC Article

    04/27/2013
    High focal axoplasmic Ca2+ levels correlate with focal aggregation of the reverse Na+/Ca2+ exchanger 1, voltage-gated N-type Ca2+ channel alpha1B subunit, and actin at the sites of spheroids in individual axons.

    Focal increases of axoplasmic Ca2+, aggregation of sodium-calcium exchanger, N-type Ca2+ channel, and actin define the sites of spheroids in axons undergoing oxidative stress.
    Barsukova AG, Forte M, Bourdette D., Free PMC Article

    11/17/2012
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