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

1. Treatment of AOAA markedly suppressed expression of NaV1.7 and NaV1.8 in DRGs of lumbar disc herniation (LDH) rats. These data suggest that targeting the CBS-H2S signaling at the DRG level might represent a novel therapeutic strategy for chronic pain relief in patients with LDH. PMID: 27905525
2. Study found that trigeminal ganglion in rats subjected to an infraorbital nerve-chronic constriction injury showed upregulation of Nav1.3 and downregulation of Nav1.7, Nav1.8, and Nav1.9 messenger RNA and protein levels. Findings suggest that voltage-gated sodium channels may participate in the regulation of trigeminal neuralgia. PMID: 27327156
3. This study demonstrated the modulation of Nav1.8 by LPA in DRG neurons, and that this probably underlies the peripheral mechanism by which bone cancer pain is induced. PMID: 27631681
4. investigated whether the aberrant expression of Nav1.8 in dorsal root ganglia contributes to generation of pain induced by scorpion stings PMID: 26764239
5. Up-regulation of Nav1.8 in nociceptive neurons contributes to persistent pain regulated by SDF1-CXCR4 signaling. PMID: 26597700
6. The study demonstrates that positive shift of Nav1.8 current inactivation curve in injured neurons causes neuropathic pain following chronic constriction injury. PMID: 26005195
7. functional upregulation of Nav1.8 channels on the membrane of DRG neurons contributes to the development of cancer-induced bone pain PMID: 25503076
8. A novel splice variant of SCN10A lacking exon 11 was found in human but not detected in mouse or rat. PMID: 24763188
9. Sodium channels Na(V)1.8 and Na(V)1.9 in primary sensory neurons played distinct roles in complete Freund's adjuvant-induced inflammatory pain.[Na(V)1.8, Na(V)1.0] PMID: 21572961
10. The results of this study indicate that histamine increases Nav1.8 expression in primary afferent neurons via H2 receptor-mediated pathway and thereby contributes to neuropathic pain PMID: 24990156
11. PKC-NF-kappaB are involved in CCL2-induced elevation of Nav1.8 current density by promoting the phosphorylation of Nav1.8 and its expression. PMID: 24724624
12. This study demonistrated that Na(v)1.8 in controlling the excitability of Abeta-fibers and its potential contribution to the development of mechanical allodynia under persistent inflammation. PMID: 24606981
13. NaV1.8 are expressed in large and small diameter sensory afferent neurons. PMID: 23064159
14. Neonatal colonic inflammation up regulates NaV1.7 and NaV1.8 expression and potentiates total Na+ channel current density in colon-specific dorsal root ganglion neurons in adult rats with visceral hypersensitivity. PMID: 23449670
15. The up-regulation of mRNA and protein levels of Nav1.8 suggested it's potential involvement in the development and maintenance of bone cancer pain. PMID: 22342308
16. Neonatal maternal deprivation remarkably enhanced expression of Na(V)1.8 at protein levels but not at mRNA levels in colon-related dorsal root ganglion neurons. PMID: 23139220
17. Data suggest that targeting the Nav1.8 sodium channel on joint nociceptors could therefore be useful for the treatment of osteoarthritis (OA) pain. PMID: 22225591
18. Spinal activation of Nav1.8 mediates induction and/or maintenance of capsaicin- and peripheral ischemia-induced mechanical allodynia and thermal hyperalgesia. PMID: 22127815
19. The beta-subunits differentially regulate the expression and gating of Nav1.8 and Nav1.6 in dorsal root ganglion neurons. PMID: 21562192
20. targeted delivery of agents that interfere with axonal NaV1.8 mRNA may represent effective neuropathic pain treatments. PMID: 21965668
21. The concomitant axonal accumulation of NaV1.8 mRNA may play a role in the pathogenesis of neuropathic pain. PMID: 19320998
22. The beta3 subunit promotes surface expression of Na(v)1.8 by masking its endoplasmic reticulum (ER)-retention/retrieval signal. PMID: 18782866
23. Time course study of dental pulp inflammation indicated that differences in relative mRNA expression levels of Nav 1.8 were correlated with the severity of inflammation. PMID: 21276017
24. The pain caused by molar extraction is related to the up-regulation of expressions of sodium channels protein Nav1.8 and Nav1.9 mRNA. PMID: 19575990
25. Findings suggest that Nav1.8 plays a role in the development and maintenance of bone cancer pain. PMID: 20482896
26. the trafficking of Na(v)1.8 is regulated by prostaglandin E(2) through the protein kinase A signaling pathway. PMID: 20028484
27. 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
28. Annexin II light chain (p11) is a regulatory factor that facilitates the expression of Na(V)1.8. p11 binds directly to the amino terminus of Na(V)1.8 and promotes the translocation of Na(V)1.8 to the plasma membrane, producing functional channels PMID: 12050667
29. conclude from mutation and electrophyiology studies that the two Na(+) channels, rNa(v)1.7 and rNa(v)1.8 (Scn10a gene), may have different endoplasmic reticulum processing signals. PMID: 14960304
30. functional behavior of Nav1.8 will vary depending on the type of beta-subunit expressed under normal and disease states PMID: 15178439
31. Nav 1.8 is involved in frank nerve injury & inflammatory pain as compared to acute, post-operative or chemotherapy-induced neuropathic pain states. PMID: 16545521
32. use-dependent reduction of Na(v)1.8 current in these two DRG subpopulations contributes to functional differences between these two neuronal populations PMID: 17108087
33. data present strong evidence for a specialized role of Na(v)1.8 in nociceptors as the critical molecule for the perception of cold pain and pain in the cold PMID: 17568746
34. Na(V)1.8 plays a role in the maintenance of chronic inflammatory pain several weeks after the initial insult PMID: 17950013
35. Low concentrations of tetrodotoxin interact with tetrodotoxin-resistant voltage-gated sodium channels. PMID: 18552876
36. This study results provide evidence for presynaptic expression of functional TTX-R Na(+) channels that may be important for shaping presynaptic action potentials and regulating transmitter release at the first sensory synapse. PMID: 19162133
37. Chimeras containing the N-terminal half of Na(v)1.8 exhibited a large response similar to wild-type Na(v)1.8, indicating that the region conferring high sensitivity to ciguatoxin action is located in the D1 or D2 domains. PMID: 19164297
38. trigeminal ganglion sodium channel transcripts mature in steps that are specific for each transcript in development PMID: 19269275
39. These findings reveal that Pdzd2 and p11 play collaborative roles in regulation of Na(V)1.8 expression in sensory neurons. PMID: 19607921

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KEGG: rno:29571

STRING: 10116.ENSRNOP00000047944

UniGene: Rn.10246