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

SCN9A encodes a voltage-gated sodium channel which plays a significant role in nociception signaling. Additionally we are shipping SCN9A Antibodies (121) and SCN9A Proteins (11) and many more products for this protein.

list all ELISA KIts Gene Name GeneID UniProt
SCN9A 20274  
SCN9A 78956 O08562
SCN9A 6335 Q15858
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Top SCN9A ELISA Kits at antibodies-online.com

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Catalog No. Reactivity Sensitivity Range Images Quantity Supplier Delivery Price Details
Human 0.1 ng/mL 0.5-10 ng/mL   96 Tests Log in to see 15 to 18 Days
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Rat 0.1 ng/mL 0.5-10 ng/mL   96 Tests Log in to see 15 to 18 Days
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More ELISA Kits for SCN9A Interaction Partners

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

  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) interaction partners

  1. 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.

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

  3. 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.

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

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

  6. 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.

  7. 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.

  8. 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.

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

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

  11. 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.

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

  13. 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

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

  15. 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

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

  17. 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

  18. 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) interaction partners

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

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

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

  4. 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.

  5. 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.

  6. 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

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

  8. 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.

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

  10. 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.

  11. 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

  12. 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.

  13. Gain-of-function mutation of a voltage-gated sodium channel NaV1.7 associated with peripheral pain and impaired limb development

  14. Results indicate that Nav 1.7 promotes gastric cancer progression through MACC1-mediated upregulation of NHE1.

  15. 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.

  16. 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

  17. Mutant cycle analysis with modified saxitoxins reveals specific interactions critical to attaining high-affinity inhibition of human NaV1.7.

  18. Postoperative pain was affected by SCN9A genetic variability in gynecological surgical patients.

  19. Patients with the SCN9A mutation with inherited erythromelalgia were characterized for the pain phenotype among individuals.

  20. These findings provided evidence that the variability of basal pain sensitivity was associated with SCN9A polymorphisms in the general population.

SCN9A Antigen Profile

Antigen Summary

This gene encodes a voltage-gated sodium channel which plays a significant role in nociception signaling. Mutations in this gene have been associated with primary erythermalgia, channelopathy-associated insensitivity to pain, and paroxysmal extreme pain disorder.

Gene names and symbols associated with SCN9A

  • sodium channel, voltage-gated, type IX, alpha subunit (SCN9A) antibody
  • sodium voltage-gated channel alpha subunit 9 (SCN9A) antibody
  • sodium channel protein type 9 subunit alpha (LOC100016648) antibody
  • sodium channel, voltage-gated, type IX, alpha (Scn9a) antibody
  • sodium voltage-gated channel alpha subunit 9 (Scn9a) antibody
  • DKFZp459G084 antibody
  • ETHA antibody
  • FEB3B antibody
  • GEFSP7 antibody
  • mKIAA4197 antibody
  • Nav1.7 antibody
  • NE-NA antibody
  • NENA antibody
  • PN1 antibody
  • Scn2a antibody
  • SCN9A antibody
  • SFNP antibody

Protein level used designations for SCN9A

sodium channel, voltage-gated, type IX, alpha subunit , sodium channel protein type 9 subunit alpha-like , peripheral sodium channel 1 , sodium channel 25 , sodium channel protein type 9 subunit alpha , sodium channel protein type IX subunit alpha , sodium channel, voltage-gated, type IX, alpha polypeptide , voltage-gated sodium channel alpha subunit Nav1.7 , voltage-gated sodium channel subunit alpha Nav1.7 , sodium channel, voltage-gated, type 9, alpha polypeptide , hNE-Na , neuroendocrine sodium channel , nas , schwann cell sodium channel , sodium channel alpha-subunit

GENE ID SPECIES
488381 Canis lupus familiaris
533065 Bos taurus
100016648 Monodelphis domestica
100172961 Pongo abelii
100385702 Callithrix jacchus
100482886 Ailuropoda melanoleuca
100516701 Sus scrofa
100583836 Nomascus leucogenys
20274 Mus musculus
78956 Rattus norvegicus
6335 Homo sapiens
100009210 Oryctolagus cuniculus
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