Sodium Channel, Voltage-Gated, Type IX, alpha Subunit (SCN9A) ELISA Kits

Cow (Bovine) Sodium Channel, Voltage-Gated, Type IX, alpha Subunit (SCN9A) Interaktionspartner

1. TNF-alpha up-regulates NaV1.7 mRNA in both adrenal chromaffin cells and dorsal root ganglia (DRG) neurons, highlighting the peripheral nociceptive mechanism of TNF-alpha

2. Findings suggest that the endothelin-1-induced down-regulation of NaV1.7 (SCN9A) diminishes NaV1.7-related catecholamine secretion and dephosphorylation of tau.

3. Nav1.7-Ca2+ influx-induced increased phosphorylations of extracellular signal-regulated kinase (ERK) and p38 attenuate tau phosphorylation via glycogen synthase kinase-3beta: priming of Nav1.7 gating by ERK and p38

4. constitutively phosphorylated/activated ERK destabilizes Na(+) channel alpha-subunit mRNA via translational event, which negatively regulates steady-state level of alpha-subunit mRNA and cell surface expression of functional Na(+) channels.

5. Na influx via scn9a converged on inhibitory phosphorylation of glycogen synthase kinase-3beta, decreasing tau phosphorylation

Mouse (Murine) Sodium Channel, Voltage-Gated, Type IX, alpha Subunit (SCN9A) Interaktionspartner

1. This study demonstrated that nav1.7 contribution to peripheral nerves pain.

2. Nav1.7, known to regulate opioid receptor efficacy, interacts with the G protein-regulated inducer of neurite outgrowth (Gprin1), an opioid receptor-binding protein, demonstrating a physical and functional link between Nav1.7 and opioid signalling.

3. the NaV1.7 channel is an important mechanism underlying hyperalgesia

4. Voltage-gated sodium channel Nav1.7 controls the efficacy and balance of heterotrimeric guanine nucleotide-binding protein-coupled receptor (GPCR)-mediated pro- and antinociceptive intracellular signaling.

5. the FGF13/Nav1.7 complex is essential for sustaining the transmission of noxious heat signals

6. this paper shows that Nav1.7, by coupling with CRMP1, mediates the axonal retrograde signaling of Sema3A in axonal guidance

7. Experiments show that integration of synaptic inputs over time by Nav1.7 is critical for body weight regulation and reveal a mechanism for synaptic control of circuits regulating long term homeostatic functions.

8. 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.

9. Global Nav1.7 knockouts showed no defects in mechanical sensitivity or overall movement yet were completely insensitive to painful tactile, thermal, and chemical stimuli and were anosmic.

10. Sodium channel Nav1.7, encoded by SCN9A, is expressed in DRG neurons and regulates their excitability.

11. a novel regulatory mechanism that utilizes CRMP2 SUMOylation to choreograph NaV1.7 trafficking.

12. 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.

13. Deleting SCN9A in both sensory and sympathetic neurons abolishes pain sensations.

14. 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

15. Nav1.7 is the dominant sodium channel in rat and mouse olfactory sensory neurons.

16. Na(v)1.7 is not only necessary for pain sensation but is also an essential requirement for odour perception in both mice and humans

17. examined the function of Na(v)1.7 (PN1) in pain pathways [Na(v)1.7]

18. 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

19. SCN2A, SCN3A, and SCN9A are expressed beneath tight junctions in subsets of taste cells. SCN3A and SCN9A are expressed in TRPM5 cells, while SCN2A was expressed in TRPM5 and PKD2L1 cells.

Human Sodium Channel, Voltage-Gated, Type IX, alpha Subunit (SCN9A) Interaktionspartner

1. SCN9A mutations resulting in greater hyperpolarizing shifts in Nav1.7 sodium channels correlated with symptom onset at younger ages and comorbidities were more common in children with SCN9A mutations.

2. This work delineates a new pathway, which involves the NF-kappaB transcription factor, SCN9A expression, plasma membrane depolarization, increased calcium, the Rb/E2F pathway and mitotic gene repression in the regulation of senescence. This work thus provides new insight into the involvement of ion channels and plasma membrane potential in the control of senescence.

3. Patients with congenital insensitivity to pain due to NaV1.7 mutations have a functional absence of nociceptors.

4. this study reports the cryo-electron microscopy structures of the human Nav1.7-beta1-beta2 complex bound to two combinations of pore blockers and gating modifier toxins (GMTs), tetrodotoxin with protoxin-II and saxitoxin with huwentoxin-IV, both determined at overall resolutions of 3.2 angstroms.

5. It demonstrates the enzyme/substrate nature of Ubc9/CRMP2 binding and identify hot spots on CRMP2 that may form the basis of future drug discovery campaigns disrupting the CRMP2-Ubc9 interaction to recapitulate allosteric regulation of NaV1.7 for pain relief.

6. F826Y mutation of Nav1.7 gene is associated with DRG neurons hyperexcitable and contributes to the pathogenesis of Erythromelalgia.

7. Common Missense Variant of SCN9A Gene Is Associated with Pain Intensity in Patients with Chronic Pain from Disc Herniation

8. Each CIP subject was homozygous for a putatively nonsense variant, R1488*, in SCN9A.

9. Zebrafish embryos, transiently overexpressing the pathogenic human SCN9A mutations, have a significantly decreased density of small-nerve fibers.

10. this study reveals an important link between painful Diabetic peripheral neuropathy and NaV1.7, suggesting that rare NaV1.7 variants may predispose patients with diabetic neuropathy to developing neuropathic pain.

11. We performed functional studies on NaV1.7 C1143F. Our study indicates the involvement of inherited SCN9A variants and partial loss-of-function of NaV1.7 channels in the etiology of rare familial ASD.

12. Nav1.7 is a substrate for Fyn kinase.

13. This study demonstrated that the higher expression Nav1.7 in human Dorsal Root Ganglion Neurons.

14. cross-talk between distinct CRMP2 posttranslational modifications is a key factor in determining NaV1.7 trafficking and localization

15. Authors introduced mutations into Nav1.7 and Nav1.6 that either enhance or impair slow inactivation (SI) in order to investigate their effects on resurgent currents. The results show that enhanced SI is accompanied by impaired resurgent currents, which suggests that SI may interfere with open-channel block.

16. 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.

17. We exploited existing technologies in a novel manner to identify selective antagonists of NaV1.7. A full-deck high-throughput screen was developed for both NaV1.7 and cardiac NaV1.5 channels using a cell-based membrane potential dye FLIPR assay

18. Genetic polymorphisms of SCN9A are associated with protection for severe neuropathy induced by oxaliplatin in digestive cancer.

19. 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.

20. the FGF13/Nav1.7 complex is essential for sustaining the transmission of noxious heat signals