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SCN9A encodes a voltage-gated sodium channel which plays a significant role in nociception signaling. Zusätzlich bieten wir Ihnen SCN9A Kits (11) und SCN9A Proteine (11) und viele weitere Produktgruppen zu diesem Protein an.
Showing 10 out of 99 products:
Mammalian Monoclonal SCN9A Primary Antibody für 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 für AA, ICC - ABIN361773
Dray: Neuropathic pain: emerging treatments. in British journal of anaesthesia 2008
Show all 4 Pubmed References
TNF-alpha (zeige TNF Antikörper) up-regulates NaV1.7 mRNA in both adrenal chromaffin cells and dorsal root ganglia (DRG) neurons, highlighting the peripheral nociceptive mechanism of TNF-alpha (zeige TNF Antikörper)
Findings suggest that the endothelin-1 (zeige EDN1 Antikörper)-induced down-regulation of NaV1.7 (SCN9A) diminishes NaV1.7-related catecholamine secretion and dephosphorylation of tau.
Nav1.7-Ca2 (zeige CA2 Antikörper)+ influx-induced increased phosphorylations of extracellular signal-regulated kinase (ERK (zeige MAPK1 Antikörper)) and p38 (zeige MAPK14 Antikörper) attenuate tau phosphorylation via glycogen synthase kinase-3beta: priming of Nav1.7 gating by ERK (zeige MAPK1 Antikörper) and p38 (zeige MAPK14 Antikörper)
constitutively phosphorylated/activated ERK (zeige MAPK1 Antikörper) destabilizes Na(+) channel alpha-subunit (zeige POLG Antikörper) mRNA via translational event, which negatively regulates steady-state level of alpha-subunit (zeige POLG Antikörper) 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
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 (zeige FGF13 Antikörper)/Nav1.7 complex is essential for sustaining the transmission of noxious heat signals
this paper shows that Nav1.7, by coupling with CRMP1 (zeige CRMP1 Antikörper), mediates the axonal retrograde signaling of Sema3A (zeige SEMA3A Antikörper) 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 (zeige PENK Antikörper) 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 (zeige DPYSL2 Antikörper) SUMOylation to choreograph NaV1.7 trafficking.
Behavioural deficits in Nav1.7/Nav1.8 (zeige SCN10A Antikörper) 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.
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 (zeige SCN5A Antikörper) 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 (zeige CA2 Antikörper)+]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 (zeige NLRC4 Antikörper), and the SCN9A mutation may be specific, if not unique to this group
A novel Nav1.9 (zeige SCN11A Antikörper) 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 (zeige MACC1 Antikörper)-mediated upregulation of NHE1 (zeige SLC9A1 Antikörper).
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
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