Recombinant Mouse Sodium channel protein type 10 subunit alpha (Scn10a), partial

1. Nav1.8 role in the inflammatory pain.CXCL13, upregulated by peripheral inflammation, acts on CXCR5 on dorsal root ganglia neurons and activates p38, which increases Nav1.8 current density and further contributes to the maintenance of inflammatory pain. PMID: 27708397
2. Data suggests that increases in the expression of Nav1.8 channels, regulatory beta1 subunits and TNF receptor 1 contribute to increased nociceptor excitability and hyperalgesia in the tumor necrosis factor transgenic mice. PMID: 28558976
3. that ectopic NaV1.8 expression precipitates depolarizing conduction failure in Charcot-Marie-Tooth disease PMID: 27215377
4. While Scn10a transcripts are not detectible in ventricular cardiomyocytes, gene deletion results in reproducible loss of late sodium current under extreme experimental conditions. However, there are no identifiable consequences of this Scn10a deletion in the intact mouse heart at usual rates. PMID: 27806966
5. Results suggest that Nav1.8 plays a role in modulating specific aspects of the retinal physiology and that starburst amacrine cells are a fundamental cellular contributor to the oscillatory potentials in mice, a clear demonstration of the dichotomy between electroretinogram b-wave and oscillatory potentials. PMID: 27984182
6. These preclinical proof-of-concept data suggest that PF-01247324, its derivatives, or other Nav1.8-selective blockers merit further study for providing symptomatic therapy for cerebellar dysfunction in MS and related disorders. PMID: 25747279
7. A novel splice variant of SCN10A lacking exon 11 was found in human but not detected in mouse or rat. PMID: 24763188
8. Nav1.8 gain-of-function point mutation contributes to intense hyperexcitability along the afferent axon within distinct sensory neuron subtypes. PMID: 24447515
9. Nav1.8 interacts with ankyrin G and they co-localize in skin nerve fibers. PMID: 24903831
10. The enhanced NaV1.8 activity are essential for the development of long-lasting hyperalgesia in acid-induced, chronic, widespread muscle pain. PMID: 24957987
11. Analysis of BAC transgenic strains harboring an engineered deletion of the enhancer within Scn10a revealed that the enhancer was essential for Scn5a expression in cardiac tissue. SCN10A variant rs6801957 modulated Scn5a expression in the heart. PMID: 24642470
12. regulation of Nav 1.8 expression and the excitability of nociceptive primary afferent neurons may be involved in the underlying mechanisms PMID: 23773488
13. Nav1.8 expression increases in dorsal root ganglion neurons following pretreatment with CC chemokine ligand 2. PMID: 22870919
14. We demonstrate that 75% of dorsal root ganglion (DRG) neurons express Na(v)1.8-Cre, including >90% of neurons expressing markers of nociceptors. PMID: 22703890
15. Behavioural deficits in Nav1.7/Nav1.8 knockout mice reflects a failure of action potential propagation in a mechanosensitive set of sensory neurons rather than a loss of primary transduction currents. PMID: 22449024
16. The functional presence of SCN10A/Nav1.8 in intracardiac neurons is demonstrated, indicating a novel role for this neuronal sodium channel in regulation of cardiac electric activity. PMID: 22723301
17. identification of enhancers in the Scn5a/Scn10a locus, regulated by TBX3 and TBX5 PMID: 22706305
18. PKCepsilon phosphorylated NaV1.8 at S1452. Alanine substitution at this site blocked PKCepsilon modulation of channel properties. NaV1.8 is an important, direct substrate of PKCepsilon that mediates PKCepsilon-dependent mechanical hyperalgesia. PMID: 22426212
19. Upregulation of Nav1.8 in cerebellum contributes to cerebellar dysfunction in multiple sclerosis and experimental autoimmune encephalomyelitis. PMID: 22367990
20. Hypermorphic mutation of the voltage-gated sodium channel encoding gene Scn10a causes a dramatic stimulus-dependent neurobehavioral phenotype. PMID: 22087007
21. Data suggest a previously unrecognized role for Nav1.8-expressing vagal neurons in gastrointestinal functions. PMID: 21618224
22. Following lumbar 5 ventral root transection there is an increase in the current densities of Nav1.8 channels, but not Nav1.9 channels in uninjured dorsal root ganglion neurons. PMID: 21145890
23. These data demonstrate that the expression of Na(v)1.8 in sensory neurons can confine the antinociceptive efficacy of lidocaine and other Na+ channel blockers employed for pain treatment. PMID: 20174994
24. Data describe alternative splicing in a NAGNAG tandem acceptor in SCN10A that results in isoforms including/lacking glutamine 1030, which is conserved among rodents and humans but its alternative usage apparently occurs with species-specific abundance. PMID: 19953341
25. The present study provides evidence for a modulatory role of Na(v)1.9, and to a lesser extent Na(v)1.8 in the development of cold, but not mechanical allodynia in neuropathic pain conditions. PMID: 19931571
26. SCN10A is expressed in mouse and human heart tissue and that PR interval is shorter in Scn10a(-/-) mice than in wild-type mice. PMID: 20062061
27. essential role in mediating spontaneous activity in sensitized nociceptors PMID: 12351708
28. The expression of sodium channel Na(v)1.8 contributes to the development of clinical deficits in an in vivo model of neuroinflammatory disease. PMID: 14533785
29. novel isoforms of Na(v)1.8 and Na(v)1.5 are each generated by alternative splicing at CAG/CAG motifs, which result in the absence or presence of predicted glutamine residues within the interdomain cytoplasmic loop IDII/III PMID: 15047701
30. Colitis-induced hyperexcitability is associated with increased slow TTX-R (Nav1.8) Na+ current. PMID: 15205116
31. Immunoblotting and RT-PCR assays showed reduced Nav1.8 levels in aged mice and loss temperature sensitivity. PMID: 15979214
32. contrast to the highly significant role for Nav1.7 in determining inflammatory pain thresholds, the development of neuropathic pain does not require the presence of either Nav1.7 or Nav1.8 alone or in combination PMID: 16111501
33. Na(v) 1.8 is either responsible for, or associated with proteins involved in mechanosensation PMID: 16478543
34. Hyperexcitability was maintained in Na(v)1.9(-/-) mice, but hyperexcitability was absent and APs were blunted in Na(v)1.8(-/-) mice. PMID: 16857712
35. These results suggest that glial cells bearing Na(x) channels are the first to sense a physiological increase in the level of sodium in body fluids, and regulate the neural activity of the CVOs by enveloping neurons. PMID: 17350991
36. The presence of Nav1.8 allows AP amplitude to be maintained in DRG neurons and their centrally projecting axons even when depolarized within the dorsal horn. PMID: 17540018
37. Mouse (Mus musculus) retina demonstrate expression of Na(v)1.8 by retinal amacrine and ganglion cells. PMID: 18399542
38. A regulatory region is identified called the sensory neuron specific restrictive element that may contain the switch for the restricted sensory neuron expression of the Nav1.8 gene product. PMID: 18466327
39. data demonstrate that Na(v)1.8-expressing neurons are essential for mechanical, cold, and inflammatory pain but not for neuropathic pain or heat sensing PMID: 18669863
40. Report involvement of voltage-gated sodium channel Na(v)1.8 in the regulation of the release and synthesis of substance P in adult mouse dorsal root ganglion neurons. PMID: 18845912
41. findings have shown that trinitrobenzenesulphonic acid colitis causes an increase in Nav 1.8 protein in colonic dorsal root ganglia neurons PMID: 19239624

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KEGG: mmu:20264

STRING: 10090.ENSMUSP00000081845

UniGene: Mm.247042