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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 ICC, IF - ABIN361773
Dray: Neuropathic pain: emerging treatments. in British journal of anaesthesia 2008
Show all 4 references for ABIN361773
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
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
Nav1.7 is the dominant sodium channel in rat and mouse olfactory sensory neurons.
examined the function of Na(v)1.7 (PN1) in pain pathways [Na(v)1.7]
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.
These findings provided evidence that the variability of basal pain sensitivity was associated with SCN9A polymorphisms in the general population.
Association of SCN9A variants with neuropathic pain and pain severity suggests a role of SCN9A in the disease etiology of neuropathic pain
We report the case of a 6-year-old girl with a SCN9A mutation who presented with both gain of function and loss of function phenotypes, including congenital corneal anesthesia.
the activity of mutant Nav1.7 channels in smooth muscle cells of skin vasculature and innervating sensory and sympathetic fibers contribute to the skin reddening
Novel SCN9A mutations altering Nav1.7 channel activation were found families with inherited erythromelalgia, paroxysmal extreme pain disorder and congenital insensitivity to pain.
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