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    Scn1b sodium channel, voltage-gated, type I, beta [ Mus musculus (house mouse) ]

    Gene ID: 20266, updated on 21-Apr-2024

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    Complex Synaptic and Intrinsic Interactions Disrupt Input/Output Functions in the Hippocampus of Scn1b Knock-Out Mice.

    Complex Synaptic and Intrinsic Interactions Disrupt Input/Output Functions in the Hippocampus of Scn1b Knock-Out Mice.
    Chancey JH, Ahmed AA, Guillén FI, Ghatpande V, Howard MA.,

    12/26/2023
    Heterogeneity of voltage gated sodium current density between neurons decorrelates spiking and suppresses network synchronization in Scn1b null mouse models.

    Heterogeneity of voltage gated sodium current density between neurons decorrelates spiking and suppresses network synchronization in Scn1b null mouse models.
    Hull JM, Denomme N, Yuan Y, Booth V, Isom LL., Free PMC Article

    06/7/2023
    Neonatal Scn1b-null mice have sinoatrial node dysfunction, altered atrial structure, and atrial fibrillation.

    Neonatal Scn1b-null mice have sinoatrial node dysfunction, altered atrial structure, and atrial fibrillation.
    Ramos-Mondragon R, Edokobi N, Hodges SL, Wang S, Bouza AA, Canugovi C, Scheuing C, Juratli L, Abel WR, Noujaim SF, Madamanchi NR, Runge MS, Lopez-Santiago LF, Isom LL., Free PMC Article

    05/28/2022
    Scn1b expression in the adult mouse heart modulates Na(+) influx in myocytes and reveals a mechanistic link between Na(+) entry and diastolic function.

    Scn1b expression in the adult mouse heart modulates Na(+) influx in myocytes and reveals a mechanistic link between Na(+) entry and diastolic function.
    Cervantes DO, Pizzo E, Ketkar H, Parambath SP, Tang S, Cianflone E, Cannata A, Vinukonda G, Jain S, Jacobson JT, Rota M., Free PMC Article

    05/14/2022
    Excitatory and inhibitory neuron defects in a mouse model of Scn1b-linked EIEE52.

    Excitatory and inhibitory neuron defects in a mouse model of Scn1b-linked EIEE52.
    Hull JM, O'Malley HA, Chen C, Yuan Y, Denomme N, Bouza AA, Anumonwo C, Lopez-Santiago LF, Isom LL., Free PMC Article

    09/25/2021
    Sodium channel beta1 subunits are post-translationally modified by tyrosine phosphorylation, S-palmitoylation, and regulated intramembrane proteolysis.

    Sodium channel β1 subunits are post-translationally modified by tyrosine phosphorylation, S-palmitoylation, and regulated intramembrane proteolysis.
    Bouza AA, Philippe JM, Edokobi N, Pinsky AM, Offord J, Calhoun JD, Lopez-Florán M, Lopez-Santiago LF, Jenkins PM, Isom LL., Free PMC Article

    01/16/2021
    Delayed maturation of GABAergic signaling in the Scn1a and Scn1b mouse models of Dravet Syndrome.

    Delayed maturation of GABAergic signaling in the Scn1a and Scn1b mouse models of Dravet Syndrome.
    Yuan Y, O'Malley HA, Smaldino MA, Bouza AA, Hull JM, Isom LL., Free PMC Article

    11/21/2020
    This study demonstrated that the sodium channel beta1 subunit proteins encoded by this mutant gene are expressed at the surface of neuronal cell bodies.

    β1-C121W Is Down But Not Out: Epilepsy-Associated Scn1b-C121W Results in a Deleterious Gain-of-Function.
    Kruger LC, O'Malley HA, Hull JM, Kleeman A, Patino GA, Isom LL., Free PMC Article

    07/8/2017
    Loss of Scn1b caused increased amplitude of tetrodotoxin-sensitive INa, delayed after-depolarizations, triggered beats, changed Ca2+ transients,and susceptibility ventricular arrhythmias.

    Scn1b deletion leads to increased tetrodotoxin-sensitive sodium current, altered intracellular calcium homeostasis and arrhythmias in murine hearts.
    Lin X, O'Malley H, Chen C, Auerbach D, Foster M, Shekhar A, Zhang M, Coetzee W, Jalife J, Fishman GI, Isom L, Delmar M., Free PMC Article

    12/19/2015
    Study showed that Scn1b is widely expressed at axon initial segments across the mouse brain, there is considerable heterogeneity in the proportion of Scn1b-positive neurons and the amount of expression between and within brain regions

    Sodium channel β1 subunit localizes to axon initial segments of excitatory and inhibitory neurons and shows regional heterogeneity in mouse brain.
    Wimmer VC, Harty RC, Richards KL, Phillips AM, Miyazaki H, Nukina N, Petrou S.

    10/3/2015
    beta1-beta3 is more likely to form a di-polymer than beta1-beta1 based on molecular interaction analysis, including potential energy analysis

    Study of the residues involved in the binding of β1 to β3 subunits in the sodium channel.
    Liu Q, Jin Y, Wang K, Meng XX, Yang Y, Yang Z, Zhao YS, Zhao MY, Zhang JH.

    10/25/2014
    Scn1b mutant subicular and layer 2/3 pyramidal neurons had increased action potential firing rates, presumably as a consequence of their increased input resistance

    Reduced dendritic arborization and hyperexcitability of pyramidal neurons in a Scn1b-based model of Dravet syndrome.
    Reid CA, Leaw B, Richards KL, Richardson R, Wimmer V, Yu C, Hill-Yardin EL, Lerche H, Scheffer IE, Berkovic SF, Petrou S.

    08/30/2014
    Stronger expressions of SCN5a, SCN1b and Kir2.1 were observed in ventricular-like and atrial-like cells compared to that of pacemaker-like cardiomyocytes.

    [Expression of Kir2.1, SCN5a and SCN1b channel genes in mouse cardiomyocytes with various electric properties: patch clamp combined with single cell RT-PCR study].
    Luo HY, Liang HM, Hu XW, Tang M.

    06/8/2013
    Scn1b is critical for neuronal proliferation, migration, and pathfinding during the critical postnatal period of brain development.

    Abnormal neuronal patterning occurs during early postnatal brain development of Scn1b-null mice and precedes hyperexcitability.
    Brackenbury WJ, Yuan Y, O'Malley HA, Parent JM, Isom LL., Free PMC Article

    03/16/2013
    The results presented here identify Navbeta1 as a component of native neuronal Kv4.2-encoded I(A) channel complexes and a novel regulator of I(A) channel densities and neuronal excitability.

    The sodium channel accessory subunit Navβ1 regulates neuronal excitability through modulation of repolarizing voltage-gated K⁺ channels.
    Marionneau C, Carrasquillo Y, Norris AJ, Townsend RR, Isom LL, Link AJ, Nerbonne JM., Free PMC Article

    06/30/2012
    Scn1b regulates the electrical excitability of nociceptive DRG neurons in vivo by modulating both I(Na) and I(K).

    Na+ channel Scn1b gene regulates dorsal root ganglion nociceptor excitability in vivo.
    Lopez-Santiago LF, Brackenbury WJ, Chen C, Isom LL., Free PMC Article

    09/10/2011
    propose reciprocity of function between Scn1b (beta1) and Na(v)1.6 such that beta1-mediated neurite outgrowth requires Na(v)1.6-mediated I(Na), and Na(v)1.6 localization and consequent high-frequency firing require beta1

    Functional reciprocity between Na+ channel Nav1.6 and beta1 subunits in the coordinated regulation of excitability and neurite outgrowth.
    Brackenbury WJ, Calhoun JD, Chen C, Miyazaki H, Nukina N, Oyama F, Ranscht B, Isom LL., Free PMC Article

    03/8/2010
    Sodium channel beta1 regulatory subunit deficiency reduces pancreatic islet glucose-stimulated insulin and glucagon secretion.

    Sodium channel beta1 regulatory subunit deficiency reduces pancreatic islet glucose-stimulated insulin and glucagon secretion.
    Ernst SJ, Aguilar-Bryan L, Noebels JL., Free PMC Article

    01/21/2010
    Voltage-gated Na(+) channel beta1 subunits signal via multiple pathways on multiple timescales and play important roles in the postnatal development of the CNS

    Voltage-gated Na+ channel beta1 subunit-mediated neurite outgrowth requires Fyn kinase and contributes to postnatal CNS development in vivo.
    Brackenbury WJ, Davis TH, Chen C, Slat EA, Detrow MJ, Dickendesher TL, Ranscht B, Isom LL., Free PMC Article

    01/21/2010
    Electrocardiograms from Scn1b knockout mice displayed longer heart rate intervals and extended long QT syndromes.

    Sodium channel Scn1b null mice exhibit prolonged QT and RR intervals.
    Lopez-Santiago LF, Meadows LS, Ernst SJ, Chen C, Malhotra JD, McEwen DP, Speelman A, Noebels JL, Maier SK, Lopatin AN, Isom LL., Free PMC Article

    01/21/2010
    Floxed allele for conditional inactivation of the voltage-gated sodium channel beta1 subunit Scn1b.

    Floxed allele for conditional inactivation of the voltage-gated sodium channel beta1 subunit Scn1b.
    Chen C, Dickendesher TL, Oyama F, Miyazaki H, Nukina N, Isom LL.

    01/21/2010
    Sodium channel beta1 subunits promote neurite outgrowth in cerebellar granule neurons

    Sodium channel beta1 subunits promote neurite outgrowth in cerebellar granule neurons.
    Davis TH, Chen C, Isom LL.

    01/21/2010
    The primary sodium channels present in ventricular myocytes are composed of Na(v)1.5 plus beta2 and/or beta4 subunits in intercalated disks and Na(v)1.1, Na(v)1.3, and Na(v)1.6 plus beta1 and/or beta3 subunits in the transverse tubules.

    Distinct subcellular localization of different sodium channel alpha and beta subunits in single ventricular myocytes from mouse heart.
    Maier SK, Westenbroek RE, McCormick KA, Curtis R, Scheuer T, Catterall WA.

    01/21/2010
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