| SIRT1 mediates the excitability of spinal CaMKIIalpha-positive neurons and participates in neuropathic pain by controlling Nav1.3. | SIRT1 mediates the excitability of spinal CaMKIIα-positive neurons and participates in neuropathic pain by controlling Nav1.3.
Wang Y, Zhang Y, Ma N, Zhao W, Ren X, Sun Y, Zang W, Cao J., Free PMC Article | 07/8/2024 |
| Nav1.3 and FGF14 are primary determinants of the TTX-sensitive sodium current in mouse adrenal chromaffin cells. | Nav1.3 and FGF14 are primary determinants of the TTX-sensitive sodium current in mouse adrenal chromaffin cells.
Martinez-Espinosa PL, Yang C, Xia XM, Lingle CJ., Free PMC Article | 10/23/2021 |
| Nav1.3 is expressed in neutrophils in vivo and regulates attachment, transmigration, and chemotaxis. | Sodium Channel Nav1.3 Is Expressed by Polymorphonuclear Neutrophils during Mouse Heart and Kidney Ischemia In Vivo and Regulates Adhesion, Transmigration, and Chemotaxis of Human and Mouse Neutrophils In Vitro.
Poffers M, Bühne N, Herzog C, Thorenz A, Chen R, Güler F, Hage A, Leffler A, Echtermeyer F. | 08/24/2019 |
| enterochromaffin (EC) cells use Scn3a-encoded voltage-gated sodium channel NaV1.3 for electrical excitability and 5-HT release. NaV1.3-dependent electrical excitability and its contribution to 5-HT release is a novel mechanism of EC cell function | Sodium channel Na(V)1.3 is important for enterochromaffin cell excitability and serotonin release.
Strege PR, Knutson K, Eggers SJ, Li JH, Wang F, Linden D, Szurszewski JH, Milescu L, Leiter AB, Farrugia G, Beyder A., Free PMC Article | 07/6/2019 |
| Novel de novo variant SCN3A-L247P was demonstrated to cause a defect in trafficking, which would be predicted to functionally reduce SCN3A activity. Consistent with the clinical observations, Scn3a+/Hyp mice display increased seizure susceptibility, hypoactivity, and impaired motor learning. | SCN3A deficiency associated with increased seizure susceptibility.
Lamar T, Vanoye CG, Calhoun J, Wong JC, Dutton SBB, Jorge BS, Velinov M, Escayg A, Kearney JA., Free PMC Article | 02/24/2018 |
| Scn3a was mapped to the QTL for febrile seizure susceptibility. | Mapping of a FEB3 homologous febrile seizure locus on mouse chromosome 2 containing candidate genes Scn1a and Scn3a.
Hessel EV, van Lith HA, Wolterink-Donselaar IG, de Wit M, Groot Koerkamp MJ, Holstege FC, Kas MJ, Fernandes C, de Graan PN. | 12/23/2017 |
| a huge difference in electrophysiological function between SCN1A and SCN3A mutations in the pore region; this might explain the more common SCN1A mutations detected in patients with epilepsy and the more severe phenotypes associated with these mutations | Electrophysiological Differences between the Same Pore Region Mutation in SCN1A and SCN3A.
Chen YJ, Shi YW, Xu HQ, Chen ML, Gao MM, Sun WW, Tang B, Zeng Y, Liao WP. | 03/12/2016 |
| these findings suggest that CpG methylation and MBD2 are involved in altering Scn3a expression during postnatal development and seizure condition. | Alteration of Scn3a expression is mediated via CpG methylation and MBD2 in mouse hippocampus during postnatal development and seizure condition.
Li HJ, Wan RP, Tang LJ, Liu SJ, Zhao QH, Gao MM, Yi YH, Liao WP, Sun XF, Long YS. | 05/2/2015 |
| the time course of declining expression of the murine embryonic sodium channel Nav 1.3 and the rise in expression of the adult sodium channel Nav 1.1 with susceptibility to epileptic seizures and increased incidence of sudden death | Correlations in timing of sodium channel expression, epilepsy, and sudden death in Dravet syndrome.
Cheah CS, Westenbroek RE, Roden WH, Kalume F, Oakley JC, Jansen LA, Catterall WA., Free PMC Article | 12/6/2014 |
| These results suggest that the GC box and CpG methylation might play important roles in regulating mouse Scn3a gene expression. | Promoter analysis of mouse Scn3a gene and regulation of the promoter activity by GC box and CpG methylation.
Deng GF, Qin JM, Sun XS, Kuang ZY, Su T, Zhao QH, Shi YW, Liu XR, Yu MJ, Yi YH, Liao WP, Long YS. | 09/3/2011 |
| SCN2A, SCN3A, and SCN9A are expressed beneath tight junctions in subsets of taste cells. SCN3A and SCN9A are expressed in TRPM5 cells, while SCN2A was expressed in TRPM5 and PKD2L1 cells. | Voltage-gated sodium channels in taste bud cells.
Gao N, Lu M, Echeverri F, Laita B, Kalabat D, Williams ME, Hevezi P, Zlotnik A, Moyer BD., Free PMC Article | 01/21/2010 |
| These data demonstrate that Nav1.3 is neither necessary nor sufficient for the development of nerve-injury related pain. | Nerve injury induces robust allodynia and ectopic discharges in Nav1.3 null mutant mice.
Nassar MA, Baker MD, Levato A, Ingram R, Mallucci G, McMahon SB, Wood JN., Free PMC Article | 01/21/2010 |