Recombinant Mouse Sodium channel protein type 8 subunit alpha (Scn8a), partial

1. we demonstrated that a selective reduction in Scn8a can dramatically protect against the development of spontaneous seizures, hyperactivity, and reactive gliosis in a mouse model of MTLE. PMID: 29317669
2. in the absence of Nav1.6 expression, the AIS is occupied by Nav1.2 channels. However, APs are generated in the AIS, and differences in AP propagation to soma and dendrites are minimal. PMID: 29991598
3. Therefore, APP modulates Nav1.6 sodium channels through a Go-coupled JNK pathway, which is dependent on phosphorylation of APP at Thr668. PMID: 28008944
4. 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. PMID: 28193882
5. 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. PMID: 28434994
6. Differential distribution in primary sensory endings suggests specialized roles for these three NaV isoforms in the process of mechanosensory signaling by muscle spindles. PMID: 28123009
7. that loss of Scn8a leads to altered thalamic reticular nucleus cell intrinsic excitability and a failure in recurrent RT synaptic inhibition PMID: 28238546
8. 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. PMID: 27836728
9. 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. PMID: 26807988
10. the presences of Nav1.1, Nav1.6, Navbeta1 and Navbeta3 mRNA and their reduced levels in rat SAN during aging. PMID: 26528804
11. 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 PMID: 26974309
12. the role of Nav1.6 in general anesthesia using two mouse mutants with reduced activity of Nav1.6, was examined. PMID: 26252017
13. observed increased hippocampal pyramidal cell excitability in heterozygous and homozygous Scn8a-R1627H mutants, and decreased interneuron excitability in heterozygous Scn8a-R1627H mutants. PMID: 26410685
14. The data support a model where ankyrinG-binding is required for preferential Nav1.6 insertion into the axon initial segment plasma membrane during development. PMID: 25874799
15. the degenerating muscle mutation is a loss of function mutation of scn8a PMID: 25380697
16. N1768D mutation of SCN8A is sufficient to induce seizures and SUDEP in knock-in mice. PMID: 25227913
17. APP enhances Nav1.6 sodium channel cell surface expression through a Go-coupled JNK pathway PMID: 25767117
18. 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 PMID: 25043721
19. 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. PMID: 24704313
20. 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. PMID: 25659151
21. 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. PMID: 24138934
22. interaction with Sin3B influences Na(v)-channel trafficking or stability in the membrane. PMID: 24077057
23. The crystal structure of apo-CaM:Na(V)1.6IQ motif, along with functional studies, are reported. PMID: 23942337
24. The findings of this study provided behavioural evidence for a crucial role of Nav1.6 in multiple peripheral pain pathways including cold allodynia. PMID: 23711479
25. Expression levels of brain Nav1.6 are increased in animals with autoimmune encephalomyelitis animals treated with sodium channel blockers. PMID: 23735284
26. 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. PMID: 23640885
27. NaV1.6 directly binds to pumilio-2 protein and results in regulation of membrane excitability. PMID: 23739961
28. Scn8a channel mediates esurgent-like currents in vas deferens myocytes. PMID: 22986623
29. This study showed that type 2 diabetes induces significant and persistent increase of Nav1.6 expression in the DRG, which may participate in the diabetic neuropathic. PMID: 22075254
30. Loss of Scn8a is associated with reduced Retinal Function. PMID: 22355369
31. Na(V)1.6 participates in excitation contraction coupling, and represents an intrinsic depolarizing reserve that contributes to excitation. PMID: 21948246
32. Voltage-gated sodium channel Nav1.6 mediates the hyperpolarizing threshold response of peripheral myelinated nerve fibers. PMID: 21295113
33. The atrophic degeneration in some fore and hind limb muscles of dmu(Scn8a) mice may increase CGRP expression in their motoneurons. PMID: 21061159
34. Nedd4-2 interacts with Na(v)1.6 via a Pro-Ser-Tyr(1945) motif in the C terminus of the channel and reduces Na(v)1.6 current density, and this regulation requires both the Pro-Gly-Ser-Pro motif in L1 and the Pro-Ser-Tyr motif in the C terminus PMID: 20530479
35. the Scn8a voltage-gated sodium channel has a role insleep architecture, diurnal corticosterone levels, and spatial memory PMID: 20353942
36. Nav1.6 channels at axon initial segments contribute to persistent Na(+) current and ensure a high degree of temporal precision in repetitive firing of cerebellar granule cells. PMID: 20173079
37. Sodium currents in vas deferens myocytes were due to activation of NaV1.6 channels and the gating properties of these channels suggest that they have a role in regulating muscle excitability, particularly in response to rapid depolarizing stimuli. PMID: 20054822
38. Complementation testing with a known Scn8a mouse mutant confirmed that this mutation is responsible for the Cloth-ears phenotype. Our findings suggest a novel role for Scn8a in peripheral neural hearing loss and paroxysmal motor dysfunction. PMID: 19737145
39. med(J) mutation shows greatly reduced levels of Scn8a voltage-gated sodium channels, causing abnormal conduction of action potentials throughout the nervous system and accounting for absence of spontaneous bursting activity in the cochlear nucleus. PMID: 12204355
40. Molecular and pathological effects of a modifier gene, Scnm1, on deficiency of the sodium channel Scn8a (Na(v)1.6), in genetic models of movement disorders. PMID: 12374766
41. Development of closed-state inactivation was also much faster for Nav1.6 currents than for Nav1.7 currents. PMID: 12843211
42. modifier mutation introduces a nonsense codon into SCNM1, a zinc finger protein and putative splice factor; the effect of the modifier mutation is to reduce the abundance of correctly spliced sodium channel transcripts below the threshold for survival PMID: 12920299
43. FHF2B, a member of the FGF homologous factor (FHF) subfamily, is an interacting partner of Na(v)1.6. PMID: 15282281
44. However, Na(v)1.2 channels show a greater accumulation of inactivation at higher frequencies of stimulation (20-100 Hz) than Na(v)1.6 and thus are likely to generate lower frequencies of firing. PMID: 15760941
45. results demonstrate for the first time the intrinsic ability of Na(v)1.6 to produce a resurgent current, and also show that cell background is critical in permitting the generation of these currents PMID: 15811336
46. Nav channels generate and regenerate action potentials at multiple sites along the cochlear ganglion cells and nerve fibers, including the afferent endings, ganglionic initial segments, and nodes of Ranvier PMID: 16033895
47. Our data supports the hypothesis that the lack of expression of Nav1.6 in Schwann cells at neuromuscular junctions might play a role in the med phenotype. PMID: 16078241
48. specialized kinetics of Purkinje Na channels depend directly on Scn8a expression PMID: 16687615
49. Beta-scorpion toxin enhance channel activaton, which could make it a model drug to replace deep brain stimulation of the subthalamic nucleus in patients with Parkinson disease. PMID: 16702217
50. Inactivation of sodium channel Scn8A (Na-sub(v)1.6) in Purkinje neurons impairs learning in Morris water maze and delay but not trace eyeblink classical conditioning. PMID: 16719687

Show More

Hide All

KEGG: mmu:20273

STRING: 10090.ENSMUSP00000080842

UniGene: Mm.385012