| Therefore, APP modulates Nav1.6 sodium channels through a Go-coupled JNK pathway, which is dependent on phosphorylation of APP at Thr668. | Amyloid precursor protein modulates Nav1.6 sodium channel currents through a Go-coupled JNK pathway.
Li S, Wang X, Ma QH, Yang WL, Zhang XG, Dawe GS, Xiao ZC., Free PMC Article | 06/23/2018 |
| The results demonstrate that Scn8a plays a vital role in neuronal excitability and provide insight into the mechanism and future treatment of epileptogenesis in early infantile epileptic encephalopathy. | Neuronal hyperexcitability in a mouse model of SCN8A epileptic encephalopathy.
Lopez-Santiago LF, Yuan Y, Wagnon JL, Hull JM, Frasier CR, O'Malley HA, Meisler MH, Isom LL., Free PMC Article | 04/14/2018 |
| Nav1.6 expression at mRNA levels in ischemic and contralateral hemispheres of middle cerebral artery occlusion (MCAO) rats were persistently decreased after reperfusion compared to sham-operated rat, but a prominent, dynamic increase of Nav1.6 immunoreactivity in reactive astrocytes was observed in the genu of corpus callosum in the acute phase. Upregulation of Nav1.6 expression strongly correlated with astrogliosis. | Transient upregulation of Nav1.6 expression in the genu of corpus callosum following middle cerebral artery occlusion in the rats.
Zhu H, Lin W, Zhao Y, Wang Z, Lao W, Kuang P, Zhou H. | 02/10/2018 |
| Differential distribution in primary sensory endings suggests specialized roles for these three NaV isoforms in the process of mechanosensory signaling by muscle spindles. | Distribution of TTX-sensitive voltage-gated sodium channels in primary sensory endings of mammalian muscle spindles.
Carrasco DI, Vincent JA, Cope TC., Free PMC Article | 09/23/2017 |
| that loss of Scn8a leads to altered thalamic reticular nucleus cell intrinsic excitability and a failure in recurrent RT synaptic inhibition | Regulation of Thalamic and Cortical Network Synchrony by Scn8a.
Makinson CD, Tanaka BS, Sorokin JM, Wong JC, Christian CA, Goldin AL, Escayg A, Huguenard JR., Free PMC Article | 09/16/2017 |
| The data of this study support the view that gain-of-function mutations of SCN8A lead to pathogenic alterations in brain function contributing to encephalopathy. | Altered gene expression profile in a mouse model of SCN8A encephalopathy.
Sprissler RS, Wagnon JL, Bunton-Stasyshyn RK, Meisler MH, Hammer MF., Free PMC Article | 05/13/2017 |
| The clinical phenotype of the severe hypomorphic sodium channel gene SCN8A mutant expands the spectrum of Scn8a disease to include a recessively inherited, chronic and progressive movement disorder. | Single amino acid deletion in transmembrane segment D4S6 of sodium channel Scn8a (Nav1.6) in a mouse mutant with a chronic movement disorder.
Jones JM, Dionne L, Dell'Orco J, Parent R, Krueger JN, Cheng X, Dib-Hajj SD, Bunton-Stasyshyn RK, Sharkey LM, Dowling JJ, Murphy GG, Shakkottai VG, Shrager P, Meisler MH., Free PMC Article | 12/17/2016 |
| the presences of Nav1.1, Nav1.6, Navbeta1 and Navbeta3 mRNA and their reduced levels in rat SAN during aging. | Age-dependent alterations of voltage-gated Na(+) channel isoforms in rat sinoatrial node.
Huang X, Du Y, Yang P, Lin S, Xi Y, Yang Z, Ma A. | 09/24/2016 |
| This study demonstrates that Nav channel expression in lumbar motoneurons is altered after SCI, and it shows a tight relationship between the calpain-dependent proteolysis of Nav1.6 channels, the upregulation of I(NaP) and spastici | Cleavage of Na(+) channels by calpain increases persistent Na(+) current and promotes spasticity after spinal cord injury.
Brocard C, Plantier V, Boulenguez P, Liabeuf S, Bouhadfane M, Viallat-Lieutaud A, Vinay L, Brocard F. | 08/27/2016 |
| the role of Nav1.6 in general anesthesia using two mouse mutants with reduced activity of Nav1.6, was examined. | Reduced Nav1.6 Sodium Channel Activity in Mice Increases In Vivo Sensitivity to Volatile Anesthetics.
Pal D, Jones JM, Wisidagamage S, Meisler MH, Mashour GA., Free PMC Article | 05/21/2016 |
| observed increased hippocampal pyramidal cell excitability in heterozygous and homozygous Scn8a-R1627H mutants, and decreased interneuron excitability in heterozygous Scn8a-R1627H mutants. | An Scn1a epilepsy mutation in Scn8a alters seizure susceptibility and behavior.
Makinson CD, Dutt K, Lin F, Papale LA, Shankar A, Barela AJ, Liu R, Goldin AL, Escayg A., Free PMC Article | 04/30/2016 |
| The data support a model where ankyrinG-binding is required for preferential Nav1.6 insertion into the axon initial segment plasma membrane during development. | Preferential targeting of Nav1.6 voltage-gated Na+ Channels to the axon initial segment during development.
Akin EJ, Solé L, Dib-Hajj SD, Waxman SG, Tamkun MM., Free PMC Article | 01/16/2016 |
| the degenerating muscle mutation is a loss of function mutation of scn8a | Glial reaction in the spinal cord of the degenerating muscle mouse (Scn8a (dmu)).
Sato T, Fujita M, Shimizu Y, Kanetaka H, Chu LW, Côté PD, Ichikawa H. | 11/14/2015 |
| N1768D mutation of SCN8A is sufficient to induce seizures and SUDEP in knock-in mice. | Convulsive seizures and SUDEP in a mouse model of SCN8A epileptic encephalopathy.
Wagnon JL, Korn MJ, Parent R, Tarpey TA, Jones JM, Hammer MF, Murphy GG, Parent JM, Meisler MH., Free PMC Article | 09/26/2015 |
| APP enhances Nav1.6 sodium channel cell surface expression through a Go-coupled JNK pathway | Amyloid precursor protein enhances Nav1.6 sodium channel cell surface expression.
Liu C, Tan FC, Xiao ZC, Dawe GS., Free PMC Article | 08/8/2015 |
| This study provided evidence for a direct link between sodium channel activity and modulation of Rac1 and ERK1/2 activation in ATP-stimulated microglia, possibly by regulating Ca(2+) transients | Contribution of sodium channels to lamellipodial protrusion and Rac1 and ERK1/2 activation in ATP-stimulated microglia.
Persson AK, Estacion M, Ahn H, Liu S, Stamboulian-Platel S, Waxman SG, Black JA. | 06/20/2015 |
| results identify the hippocampus as an important structure in the mediation of Scn8a-dependent seizure protection and suggest that selective targeting of Scn8a activity might be efficacious in patients with epilepsy. | Role of the hippocampus in Nav1.6 (Scn8a) mediated seizure resistance.
Makinson CD, Tanaka BS, Lamar T, Goldin AL, Escayg A., Free PMC Article | 05/16/2015 |
| identified the PI3K/Akt pathway, the cell-cycle regulator Wee1 kinase, and protein kinase C (PKC) as prospective regulatory nodes of neuronal excitability through modulation of the FGF14:Nav1.6 complex. | Identifying a kinase network regulating FGF14:Nav1.6 complex assembly using split-luciferase complementation.
Hsu WC, Nenov MN, Shavkunov A, Panova N, Zhan M, Laezza F., Free PMC Article | 04/4/2015 |
| In scn8a mutants, a 20-min acute restraint stress administered in the morning increases the frequency of spontaneous spike-wave discharges. Scn8a mutants also show increased anxiety-like behavior in mildly stressful situations. | Scn8a voltage-gated sodium channel mutation alters seizure and anxiety responses to acute stress.
Sawyer NT, Papale LA, Eliason J, Neigh GN, Escayg A., Free PMC Article | 08/9/2014 |
| interaction with Sin3B influences Na(v)-channel trafficking or stability in the membrane. | Interaction between the transcriptional corepressor Sin3B and voltage-gated sodium channels modulates functional channel expression.
Vega AV, Avila G, Matthews G., Free PMC Article | 05/3/2014 |
| The crystal structure of apo-CaM:Na(V)1.6IQ motif, along with functional studies, are reported. | Structural basis for the modulation of the neuronal voltage-gated sodium channel NaV1.6 by calmodulin.
Reddy Chichili VP, Xiao Y, Seetharaman J, Cummins TR, Sivaraman J., Free PMC Article | 05/3/2014 |
| The findings of this study provided behavioural evidence for a crucial role of Nav1.6 in multiple peripheral pain pathways including cold allodynia. | An animal model of oxaliplatin-induced cold allodynia reveals a crucial role for Nav1.6 in peripheral pain pathways.
Deuis JR, Zimmermann K, Romanovsky AA, Possani LD, Cabot PJ, Lewis RJ, Vetter I., Free PMC Article | 03/22/2014 |
| Expression levels of brain Nav1.6 are increased in animals with autoimmune encephalomyelitis animals treated with sodium channel blockers. | Block of a subset of sodium channels exacerbates experimental autoimmune encephalomyelitis.
Stevens M, Timmermans S, Bottelbergs A, Hendriks JJ, Brône B, Baes M, Tytgat J. | 10/19/2013 |
| inhibition of GSK3 reduces the assembly of the FGF14.Nav channel complex, modifies FGF14-dependent regulation of Na(+) currents, and induces dissociation and subcellular redistribution of the native FGF14.Nav channel complex in hippocampal neurons. | The fibroblast growth factor 14·voltage-gated sodium channel complex is a new target of glycogen synthase kinase 3 (GSK3).
Shavkunov AS, Wildburger NC, Nenov MN, James TF, Buzhdygan TP, Panova-Elektronova NI, Green TA, Veselenak RL, Bourne N, Laezza F., Free PMC Article | 09/14/2013 |
| NaV1.6 directly binds to pumilio-2 protein and results in regulation of membrane excitability. | Pumilio-2 regulates translation of Nav1.6 to mediate homeostasis of membrane excitability.
Driscoll HE, Muraro NI, He M, Baines RA., Free PMC Article | 08/10/2013 |