SCN10A Antibody, FITC conjugated

1. These data suggest that genetic variation in SCN10A may play an important role in predicting atrial fibrillation recurrence after catheter ablation in the Chinese Han population. PMID: 28281580
2. the variant rs6801957 and enhancer A may affect SCN10A gene expression and play an important role in human mechanical pain sensitivity. PMID: 29448912
3. The possible involvement of the SCN10A variant in AF development in Chinese Han populations. PMID: 27725708
4. Our findings suggest that there are interaction effects of DM and SCN10A (rs7375036) that influence the development of CAN. PMID: 27729462
5. This study demonstrated that at the association and mechanistic levels, the SCN10A single nucleotide polymorphism rs6795970 biases human pain sensitivity. PMID: 27590072
6. We investigated the association of SCN10A gene variants with 105 sporadic sudden unexplained nocturnal death syndrome victims. A total of 6 rare mutations and 16 polymorphisms were detected in SUNDS victims. This is the first report of common and rare variants of SCN10A gene in the Chinese Han population, which provides the genetic epidemiological evidence that SCN10A may be a novel susceptibility gene. PMID: 27272739
7. Compared with Brugada syndrome (BrS) patients carrying SCN5A or CACNA1C mutations, symptomatic patients in the SCN10A group tended to be older than those in the other gene groups. In six BrS probands who carried SCN10A variants, most experienced severe arrhythmic attacks. PMID: 25842276
8. The p.M650K mutation shifted steady-state fast inactivation of Nav1.8 (SCN10A)to more hyperpolarized potentials and did not significantly alter any other tested gating behaviors. The AP half-width was significantly broader and the stimulated action potential firing rate was reduced for M650K transfected DRGs compared to WT. PMID: 27598514
9. SCN10A mutations do not play primary role in arrhythmogenic right ventricular dysplasia/cardiomyopathy. PMID: 26733327
10. SCN10A genetic variation substantially influences functional status in patients with multiple sclerosis. PMID: 26740675
11. SCN10A gene mutations that reduce sodium channel current may provide a mechanistic link between Atrioventricular nodal reentrant tachycardia and Brugada syndrome and predispose to expression of both phenotypes. PMID: 25998140
12. The results demonstrate distinct properties of human Na(v)1.8, which contribute to the firing properties of human DRG neurons. PMID: 25787950
13. The common SNP SCN10A V1073 was strongly associated with Brugada syndrome and demonstrated loss of NaV1.8 function, as did rare variants in isolated patients. PMID: 25691538
14. study suggests that SCN10A variations are involved in the genesis of AF. PMID: 25691686
15. Rare SCN10A variants may contribute to atrial fibrillation susceptibility. PMID: 25053638
16. The rs6795970 in the SCN10A gene, which is reported to carry a high risk of heart block, might be associated with cardiac conduction abnormalities in Hypertrophic Cardiomyopathy patients. PMID: 26104176
17. A novel splice variant of SCN10A lacking exon 11 was found in human but not detected in mouse or rat. PMID: 24763188
18. SCN10A SNPs modulate PR interval and heart rate response during atrial fibrillation. PMID: 24072447
19. As a major susceptibility gene for Brugada syndrome (BrS), SCN10A greatly enhances the genotyping and risk stratifying of probands and BrS family members. PMID: 24998131
20. This study reports a mutation of NaV1.8 which impairs inactivation, in patients with painful idiopathic small fibre neuropathy. PMID: 24006052
21. The results demonstrate that Nav1.8 and Nav1.9 are present in human lingual nerve neuromas, with significant correlations between the level of expression of Nav1.8 and symptoms of pain. PMID: 24144460
22. Results verify that the Na+ channel Na v1.8 is present in human sperm cells and participates in the regulation of sperm function. PMID: 24086692
23. I1706V mutation associated with small-fiber neuropathy decreases current threshold and increases the firing frequency of evoked action potentials within small DRG neurons. PMID: 23986244
24. Single nucleotide polymorphism of TRPV1 315G>C, rs5981521 of pri-miR-325 and SCN10A is related to the development of functional dyspepsia. This involvement differed between Helicobater pylori-positive and -negative patients. PMID: 23047628
25. We found that SCN10A 3218 CC homozygosity with the 2884 G and 3275 C alleles was significantly associated with a reduced risk for the development of functional dyspepsia. PMID: 22618805
26. Mutations of Na(v)1.8 contribute to painful peripheral neuropathy. PMID: 23115331
27. sodium channel Na(v)1.8 is present in sensory nerves and cardiomyocytes of human heart PMID: 21646736
28. Transmembrane segments prevent surface expression of sodium channel Nav1.8 and promote calnexin-dependent channel degradation PMID: 20720009
29. 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
30. Ret-Na(v)1.8 conditional knockout mice have increased sensitivity to cold and increased formalin-induced pain, demonstrating that Ret signaling modulates the function of nociceptors in vivo. PMID: 20237269
31. Nav1.8 downregulation may be one of the pathophysiological mechanisms involved in limb lengthening-induced neuropathy. PMID: 19877286
32. Aquaporin-1 tunes pain perception by interaction with Na(v)1.8 Na+ channels in dorsal root ganglion neurons. PMID: 20018876
33. 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
34. A high capacity assay is sensitive to known state-dependent NaV1 modulators and can be used to identify novel and selective inhibitors. PMID: 16506887
35. calmodulin associates with a sodium channel, Nav1.8, in native neurons, and demonstrates a regulation of Nav1.8 currents that can significantly affect electrogenesis of DRG neurons in which Nav1.8 is normally expressed PMID: 16598065
36. 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
37. Data suggest differing, but partially overlapping, areas of binding of A-803467 and tetracaine in the Na(V)1.8 sodium channel. PMID: 19233853
38. activation of NK-1 receptor potentiates Na(v)1.8 sodium current via PKCepsilon-dependent signaling pathway, probably participating in the generation of inflammatory hyperalgesia PMID: 19563686

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HGNC: 10582

OMIM: 604427

KEGG: hsa:6336

STRING: 9606.ENSP00000390600

UniGene: Hs.250443