anti-Sodium Channel, Voltage-Gated, Type X, alpha Subunit (SCN10A) Antibodies

Mouse (Murine) Sodium Channel, Voltage-Gated, Type X, alpha Subunit (SCN10A) interaction partners

1. We find that approximately 80% of neurons responsive to cold down to 1 degrees C do not express NaV1.8, and that the genetic deletion of NaV1.8 does not affect the relative number, distribution, or maximal response of cold-sensitive neurons. Furthermore, the deletion of NaV1.8 had no observable effect on transient cold-induced (>/=5 degrees C) behaviors in mice, as measured by the cold-plantar, cold-plate (5 and 10 deg...

2. 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.

3. 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.

4. that ectopic NaV1.8 expression precipitates depolarizing conduction failure in Charcot-Marie-Tooth disease

5. 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.

6. 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.

7. 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.

8. A novel splice variant of SCN10A lacking exon 11 was found in human but not detected in mouse or rat.

9. Nav1.8 gain-of-function point mutation contributes to intense hyperexcitability along the afferent axon within distinct sensory neuron subtypes.

10. Nav1.8 interacts with ankyrin G and they co-localize in skin nerve fibers.

11. The enhanced NaV1.8 activity are essential for the development of long-lasting hyperalgesia in acid-induced, chronic, widespread muscle pain.

12. 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.

13. regulation of Nav 1.8 expression and the excitability of nociceptive primary afferent neurons may be involved in the underlying mechanisms

14. Nav1.8 expression increases in dorsal root ganglion neurons following pretreatment with CC chemokine ligand 2.

15. We demonstrate that 75% of dorsal root ganglion (DRG) neurons express Na(v)1.8-Cre, including >90% of neurons expressing markers of nociceptors.

16. 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.

17. 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.

18. identification of enhancers in the Scn5a/Scn10a locus, regulated by TBX3 and TBX5

19. These results demonstrate increased expression levels of Nav1.7, Nav1.8, and perhaps Nav1.1 in the dorsal root ganglia in mice with a heterozygous mutation of the Nf1 gene

20. 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.

Human Sodium Channel, Voltage-Gated, Type X, alpha Subunit (SCN10A) interaction partners

1. These findings suggest an association between genetic variation in SCN10A, the late sodium current, and alterations in cardiac conduction.

2. Genotype AA of the SCN10A gene is associated with a predisposition to the development of idiopathic sick sinus syndrome

3. Genotype AA of the SCN10A gene is associated with a predisposition to the development of Sick Sinus Syndrome

4. the neuronal sodium channel NaV 1.8 is up-regulated on mRNA and protein level in the human hypertrophied myocardium. Furthermore, inhibition of NaV 1.8 reduced augmented INaL , abbreviated the action potential duration, and decreased the SR-Ca(2+) leak.

5. 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.

6. the variant rs6801957 and enhancer A may affect SCN10A gene expression and play an important role in human mechanical pain sensitivity.

7. The possible involvement of the SCN10A variant in AF development in Chinese Han populations.

8. Our findings suggest that there are interaction effects of DM and SCN10A (rs7375036) that influence the development of CAN.

9. This study demonstrated that at the association and mechanistic levels, the SCN10A single nucleotide polymorphism rs6795970 biases human pain sensitivity.

10. 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.

11. 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.

12. 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.

13. SCN10A mutations do not play primary role in arrhythmogenic right ventricular dysplasia/cardiomyopathy.

14. SCN10A genetic variation substantially influences functional status in patients with multiple sclerosis.

15. 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.

16. The results demonstrate distinct properties of human Na(v)1.8, which contribute to the firing properties of human DRG neurons.

17. 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.

18. study suggests that SCN10A variations are involved in the genesis of AF.

19. Rare SCN10A variants may contribute to atrial fibrillation susceptibility.

20. 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.