S2196
Anti-Sodium Channel NaV1.9 antibody produced in rabbit
affinity isolated antibody, lyophilized powder
Synonym(s):
Anti-NAN, Anti-SNS2
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About This Item
Recommended Products
biological source
rabbit
Quality Level
conjugate
unconjugated
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
form
lyophilized powder
species reactivity
rat
technique(s)
western blot: 1:200 using rat DRG lysates
UniProt accession no.
shipped in
wet ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... SCN11A(11280)
mouse ... Scn11a(24046)
rat ... Scn11a(29701)
General description
Sodium Channel NaV1.9 is a threshold channel, that is expressed in dorsal root ganglion neurons , peripheral nociceptive neurons and visceral afferents. It is also called as SNS and NaN. It is encoded by SCN11A (sodium voltage-gated channel subunit 11) and is located on human chromosome 3p22.
Immunogen
peptide CNGDLSSLDVAKVKVHND corresponding to residues 1748-1765 of rat Nav1.9. This sequence has 15/18 residues identical in mouse and 14/18 residues identical in human.
Biochem/physiol Actions
Sodium Channel NaV1.9 participates in pain at the time of inflammation. Downregulation of Nav1.9 is observed in Hirschsprung′s disease.
Physical form
Lyophilized from phosphate buffered saline, pH 7.4, with 1% bovine serum albumin, and 0.05% sodium azide.
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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Storage Class Code
11 - Combustible Solids
WGK
WGK 2
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
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Biology and management of histologic transformation of indolent lymphoma
Freedman AS, et al.
Hematology / the Education Program of the American Society of Hematology. American Society of Hematology. Education Program, 314-20 (2005)
Decreased Nav1.9 channel expression in Hirschsprung's disease
O'Donnell AM, et al.
Journal of Pediatric Surgery, 51(9), 1458-1461 (2016)
Congenital insensitivity to pain: Fracturing without apparent skeletal pathobiology caused by an autosomal dominant, second mutation in SCN11A encoding voltage-gated sodium channel 1.9
Phatarakijnirund V, et al.
Bone, 84, 289-298 (2016)
Sodium channel NaV1.9 mutations associated with insensitivity to pain dampen neuronal excitability
Huang J, et al.
The Journal of Clinical Investigation, 127(7), 2805-2814 (2017)
Patrick Delmas et al.
Trends in neurosciences, 26(2), 55-57 (2003-01-22)
Voltage-gated Na(+) channels play key roles in generating and propagating action potentials. Their gating is believed to rely exclusively on changes in membrane potential. However, recent data from Blum, Kafitz and Konnerth provide direct evidence that the opening of Na(v)1.9
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