SCN9A Antibody, FITC conjugated

1. Nav1.7 is a substrate for Fyn kinase. PMID: 29790812
2. This study demonstrated that the higher expression Nav1.7 in human Dorsal Root Ganglion Neurons. PMID: 28424991
3. cross-talk between distinct CRMP2 posttranslational modifications is a key factor in determining NaV1.7 trafficking and localization PMID: 27940916
4. Hereditary Small fiber neuropathy has been described with pathogenic mutations in sodium channels [Nav1.7 (mostly), which lead to hyperexcitability of dorsal root ganglions. These gain-of-function mutations result in degeneration of small fibers. PMID: 28639956
5. Genetic polymorphisms of SCN9A are associated with protection for severe neuropathy induced by oxaliplatin in digestive cancer. PMID: 28103821
6. the results of this study provide mechanistic evidence for a time-dependent increase in intracellular [Ca2+]i and energetic compromise in the neurites of dorsal root ganglia neurons expressing G856D mutant Nav1.7 channels. PMID: 27821467
7. the FGF13/Nav1.7 complex is essential for sustaining the transmission of noxious heat signals PMID: 28162808
8. This study showed that gain-of-function attributes at the channel level and differential effects of physiologically relevant thermal stimuli on the excitability of DRG neurons expressing mutant and WT Nav1.7 channels, suggesting a cellular mechanism for warmth-triggered pain episodes in Erythromelalgia patients. PMID: 27413160
9. The four congenital insensitivity to pain families, while not closely related, belong to the same ethnic group and clan, and the SCN9A mutation may be specific, if not unique to this group PMID: 27747863
10. A novel Nav1.9 mutation, p.Arg222His, was identified in patients with early-onset pain in distal extremities including joints and gastrointestinal disturbances, but was absent from an asymptomatic blood relative. PMID: 27503742
11. Gain-of-function mutation of a voltage-gated sodium channel NaV1.7 associated with peripheral pain and impaired limb development PMID: 28381558
12. Results indicate that Nav 1.7 promotes gastric cancer progression through MACC1-mediated upregulation of NHE1. PMID: 27529686
13. This is the first study to demonstrate that binding of ProTx-II to the lipid membrane is directly linked to its potency as an hNaV1.7 channel inhibitor. PMID: 27311819
14. report the engineering of highly potent and selective inhibitors of the Nav1.7 channel based on tarantula ceratotoxin-1 (CcoTx1). We utilized a combination of directed evolution, saturation mutagenesis, chemical modification, and rational drug design to obtain higher potency and selectivity to the Nav1.7 channel PMID: 27129258
15. Mutant cycle analysis with modified saxitoxins reveals specific interactions critical to attaining high-affinity inhibition of human NaV1.7. PMID: 27162340
16. Postoperative pain was affected by SCN9A genetic variability in gynecological surgical patients. PMID: 26752484
17. Patients with the SCN9A mutation with inherited erythromelalgia were characterized for the pain phenotype among individuals. PMID: 26920677
18. These findings provided evidence that the variability of basal pain sensitivity was associated with SCN9A polymorphisms in the general population. PMID: 26168879
19. Nav1.7 deletion has profound effects on gene expression, leading to an upregulation of enkephalin precursor Penk mRNA and met-enkephalin protein in sensory neurons. PMID: 26634308
20. Association of SCN9A variants with neuropathic pain and pain severity suggests a role of SCN9A in the disease etiology of neuropathic pain PMID: 25585270
21. We report the case of a 6-year-old girl with a SCN9A mutation who presented with both gain of function and loss of function phenotypes, including congenital corneal anesthesia. PMID: 26486037
22. the activity of mutant Nav1.7 channels in smooth muscle cells of skin vasculature and innervating sensory and sympathetic fibers contribute to the skin reddening PMID: 25957174
23. The co-segregation of the I739V variant in the affected members of the family provides evidence, for the first time, that paroxysmal itch can be related to a mutation in sodium channel gene. PMID: 24820863
24. Novel SCN9A mutations altering Nav1.7 channel activation were found families with inherited erythromelalgia, paroxysmal extreme pain disorder and congenital insensitivity to pain. PMID: 25995458
25. NaV1.7 is expressed in both dorsal root ganglion neurons and pancreatic beta cells.Vulnerability of dorsal root ganglia neurons due to NaV1.7 mutations increases risk of neuropathy. PMID: 25008557
26. Our study demonstrates an example of predicting the treatment effect of mexiletine in patients suffering from a specific gain-of-function mutation in NaV1.7 PMID: 24866741
27. Nav1.7 mutations are associated with pain syndromes including erythromelalgia. PMID: 25575597
28. The novel p.L1612P Nav1.7 mutation expands the paroxysmal extreme pain disorder spectrum with a unique combination of clinical symptoms and electrophysiological properties PMID: 25285947
29. PKC can increase sodium resurgent currents through phosphorylation of a conserved Serine residue located in the domain III-IV linker of hNav1.7 PMID: 25240195
30. Sodium channel Nav1.7, encoded by SCN9A, is expressed in DRG neurons and regulates their excitability. PMID: 25209274
31. Recent studies have shown that mutations in the SCN9A gene are the cause of a subgroup of idiopathic small fiber neuropathies and that polymorphisms of SCN9A are associated with an increase in susceptibility to pain. PMID: 24202110
32. This study show a linear correlation between the level of Nav1.7 conductance and current threshold in DRG neurons. PMID: 24401712
33. EGF/EGFR-mediated upregulation of Nav1.7 is necessary for invasive behaviour in these cells. PMID: 23986482
34. A working link between nociception and olfaction via Nav1.7 in the gain-of-function direction. PMID: 23874707
35. persistent and resurgent currents are likely to determine whether a mutation in Nav1.7 leads to IEM or PEPD. PMID: 24311784
36. This study demonstrated that a variant of NaV1.7 associated with painful neuropathy depolarizes resting membrane potential and produces an enhanced inward current during interspike intervals, thereby contributing to DRG neuron hyperexcitability PMID: 23850641
37. Role of the SCN9A mutations in genetic epilepsy with febrile seizures plus and Dravet syndrome PMID: 23895530
38. 2 gain-of-function mutations in the 4th domain of Nav1.7, A1746G & W1538R, caused hyperpolarization and affected age of erythromelalgia onset. PMID: 23292638
39. Data indicate that micro-SLPTX-Ssm6a, a unique 46-residue peptide from centipede venom, potently inhibits NaV1.7. PMID: 24082113
40. a novel regulatory mechanism that utilizes CRMP2 SUMOylation to choreograph NaV1.7 trafficking. PMID: 23836888
41. More patients have suffered dyskinesis pain. A 3448 (C/T) mutation of SCN9A gene may be related to pathogenesis of pain in Parkinsonism. PMID: 23450472
42. A novel SCN9A mutation responsible for primary erythromelalgia and is resistant to the treatment of sodium channel blockers. PMID: 23383113
43. Structural and functional demonstration of the importance of radial tuning of the sodium channel S6 helix for the channel activation. PMID: 23536180
44. Patients carrying the SCN9A 3312Tallele presented with lower postoperative pain sensitivity in the presence of a similar surgical pain stimulus PMID: 23364568
45. We identified a novel homozygous mutation in SCN9A from 2 Japanese families with autosomal recessive hereditary sensory and autonomic neuropathy type IId. PMID: 23596073
46. We also found a splicing junction variant of SCN91 in all 19 patients WITH enital insensitivity to pain PMID: 23129781
47. In small-fiber neuropathy, [isoleucine]228[methionine] variant Nav1.7 channel contributes to impaired regeneration and degeneration of sensory axons. PMID: 23280954
48. Structural modelling reveals that Na(v)1.7-S241T is ~2.4 A apart from V400M in the folded channel, and thermodynamic analysis demonstrates energetic coupling of V400M and S241T during activation. PMID: 23149731
49. These data strongly suggest that pain perception in at least a subset of patients with interstitial cystitis/bladder pain syndrome is influenced by the rs6746030 polymorphism in the SCN9A voltage-gated sodium channel. PMID: 23102778
50. Splicing can change the way that Na(V) channels interact with beta subunits. PMID: 22911851

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HGNC: 10597

OMIM: 133020

KEGG: hsa:6335

STRING: 9606.ENSP00000386306

UniGene: Hs.439145