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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 (11) and SCN9A Proteins (11) and many more products for this protein.
Showing 10 out of 95 products:
Hamster Monoclonal SCN9A Primary Antibody for AA, ICC - ABIN361773
Dray: Neuropathic pain: emerging treatments. in British journal of anaesthesia 2008
Show all 4 references for 361773
Human Polyclonal SCN9A Primary Antibody for IHC, ELISA - ABIN1535378
Cox, Reimann, Nicholas, Thornton, Roberts, Springell, Karbani, Jafri, Mannan, Raashid, Al-Gazali, Hamamy, Valente, Gorman, Williams, McHale, Wood, Gribble, Woods: An SCN9A channelopathy causes congenital inability to experience pain. in Nature 2006
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 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.
Deleting SCN9A in both sensory and sympathetic neurons abolishes pain sensations.
These results demonstrate increased expression levels of Nav1.7, Nav1.8 (show SCN10A Antibodies), and perhaps Nav1.1 (show SCN1A Antibodies) in the dorsal root ganglia in mice with a heterozygous mutation of the Nf1 (show NF1 Antibodies) gene
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
A novel Nav1.9 (show SCN11A Antibodies) 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.
Gain-of-function mutation of a voltage-gated sodium channel NaV1.7 associated with peripheral pain and impaired limb development
Results indicate that Nav 1.7 promotes gastric cancer progression through MACC1 (show MACC1 Antibodies)-mediated upregulation of NHE1 (show SLC9A1 Antibodies).
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
Mutant cycle analysis with modified saxitoxins reveals specific interactions critical to attaining high-affinity inhibition of human NaV1.7.
Postoperative pain was affected by SCN9A genetic variability in gynecological surgical patients.
Patients with the SCN9A mutation with inherited erythromelalgia were characterized for the pain phenotype among individuals.
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