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SCN9A encodes a voltage-gated sodium channel which plays a significant role in nociception signaling. Additionally we are shipping SCN9A Kits (12) and SCN9A Proteins (11) and many more products for this protein.
Showing 10 out of 127 products:
Mammalian Monoclonal SCN9A Primary Antibody for ISt, IHC - ABIN1304843
Vandael, Ottaviani, Legros, Lefort, Guérineau, Allio, Carabelli, Carbone: Reduced availability of voltage-gated sodium channels by depolarization or blockade by tetrodotoxin boosts burst firing and catecholamine release in mouse chromaffin cells. in The Journal of physiology 2015
Show all 16 Pubmed References
Hamster Monoclonal SCN9A Primary Antibody for AA, ICC - ABIN361773
Dray: Neuropathic pain: emerging treatments. in British journal of anaesthesia 2008
Show all 4 Pubmed References
TNF-alpha (show TNF Antibodies) up-regulates NaV1.7 mRNA in both adrenal chromaffin cells and dorsal root ganglia (DRG) neurons, highlighting the peripheral nociceptive mechanism of TNF-alpha (show TNF Antibodies)
Findings suggest that the endothelin-1 (show EDN1 Antibodies)-induced down-regulation of NaV1.7 (SCN9A) diminishes NaV1.7-related catecholamine secretion and dephosphorylation of tau.
Nav1.7-Ca2 (show CA2 Antibodies)+ influx-induced increased phosphorylations of extracellular signal-regulated kinase (ERK (show MAPK1 Antibodies)) and p38 (show MAPK14 Antibodies) attenuate tau phosphorylation via glycogen synthase kinase-3beta: priming of Nav1.7 gating by ERK (show MAPK1 Antibodies) and p38 (show MAPK14 Antibodies)
constitutively phosphorylated/activated ERK (show MAPK1 Antibodies) destabilizes Na(+) channel alpha-subunit (show POLG Antibodies) mRNA via translational event, which negatively regulates steady-state level of alpha-subunit (show POLG Antibodies) mRNA and cell surface expression of functional Na(+) channels.
Na influx via scn9a converged on inhibitory phosphorylation of glycogen synthase kinase-3beta, decreasing tau phosphorylation
the NaV1.7 channel is an important mechanism underlying hyperalgesia
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.
the FGF13 (show FGF13 Antibodies)/Nav1.7 complex is essential for sustaining the transmission of noxious heat signals
this paper shows that Nav1.7, by coupling with CRMP1 (show CRMP1 Antibodies), mediates the axonal retrograde signaling of Sema3A (show SEMA3A Antibodies) in axonal guidance
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.
Nav1.7 deletion has profound effects on gene expression, leading to an upregulation of enkephalin precursor Penk (show PENK Antibodies) mRNA and met-enkephalin protein in sensory neurons.
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.
Sodium channel Nav1.7, encoded by SCN9A, is expressed in DRG neurons and regulates their excitability.
a novel regulatory mechanism that utilizes CRMP2 (show DPYSL2 Antibodies) SUMOylation to choreograph NaV1.7 trafficking.
Behavioural deficits in Nav1.7/Nav1.8 (show SCN10A Antibodies) knockout mice reflects a failure of action potential propagation in a mechanosensitive set of sensory neurons rather than a loss of primary transduction currents.
This study demonstrated that the higher expression Nav1.7 in human Dorsal Root Ganglion Neurons.
cross-talk between distinct CRMP2 (show DPYSL2 Antibodies) posttranslational modifications is a key factor in determining NaV1.7 trafficking and localization
Authors introduced mutations into Nav1.7 and Nav1.6 (show SCN8A Antibodies) 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.
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.
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 (show SCN5A Antibodies) channels using a cell-based membrane potential dye FLIPR assay
Genetic polymorphisms of SCN9A are associated with protection for severe neuropathy induced by oxaliplatin in digestive cancer.
the results of this study provide mechanistic evidence for a time-dependent increase in intracellular [Ca2 (show CA2 Antibodies)+]i and energetic compromise in the neurites of dorsal root ganglia neurons expressing G856D mutant Nav1.7 channels.
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.
The four congenital insensitivity to pain families, while not closely related, belong to the same ethnic group and clan (show NLRC4 Antibodies), and the SCN9A mutation may be specific, if not unique to this group
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.
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
, neuroendocrine sodium channel
, schwann cell sodium channel
, sodium channel alpha-subunit