Mouse Anti-Human Nav1.7 Monoclonal IgG1; Nav1.7 Antibody: Dylight 594; ETHA Antibody; hNE Na Antibody; NE NA Antibody; PN1 Antibody; SCN9A Antibody; voltage gated sodium channel subunit alpha Nav1 Antibody; peripheral sodium channel 1 Antibody; neuroendocrine sodium channel Antibody

For Research Use Only. Not for use in diagnostic procedures.

Monoclonal

IgG1

S68-6

Mouse

Detects ~230 kDa. No cross-reactivity against other Nav channels.

Protein G Purified

PBS pH 7.4, 50% Glycerol, 0.09% Sodium Azide

1 mg/ml (lot specific)

Store at-20 degree C.

Small volumes of anti-Nav1.7 antibody vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

Nav1.7 is a voltage-gated sodium channel and plays a critical role in the generation and conduction of action potentials and is thus important for electrical signaling by most excitable cells. Therapeutically, the association of pain insensitivity with the loss of function of a certain sodium channel may have implications. Since Nav1.7 is not present in cardiac muscle or neurons in the central nervous system, blockers of Nav1.7 will not have direct action on these cells and thus can have less side effects than current pain medications. By performing more studies, there is a possibility to develop a new generation of drugs that can reduce the pain intensity in animals (1-3).

Neuroscience; Ion Channels; Sodium Channels; Voltage-Gated Sodium Channels; Cancer; Cell Signaling

Western Blot (WB), Immunocytochemistry (ICC), Immunofluorescence (IF), Immunoprecipitation (IP), Antibody Microarray (AM)

WB: 1:1000
IHC: 1:1000
ICC/IF: 1:100

Immunohistochemistry analysis using Mouse Anti-Nav1.7 Sodium Channel Monoclonal Antibody, Clone S68-6 at 1:1000. Secondary Antibody: HRP/DAB Detection System: Biotinylated Goat Anti-Mouse, Streptavidin Peroxidase, DAB Chromogen (brown). Counterstain: Mayer Hematoxylin (purple/blue) nuclear stain.

Western Blot analysis of hamster CHO cells showing detection of Nav1.7 Sodium Channel protein using Mouse Anti-Nav1.7 Sodium Channel Monoclonal Antibody, Clone S68-6 at 1:1000 for 2 hours at RT. Secondary Antibody: Sheep Anti-Mouse IgG: HRP for 1 hour at RT.

Immunohistochemistry analysis using Mouse Anti-Nav1.7 Sodium Channel Monoclonal Antibody, Clone S68-6 at 1:1000 for 1 hour at RT. Secondary Antibody: FITC Goat Anti-Mouse (green) at 1:50 for 1 hour at RT.

Immunohistochemistry analysis using Mouse Anti-Nav1.7 Sodium Channel Monoclonal Antibody, Clone S68-6 at 1:100 for 1 hour at RT. Secondary Antibody: FITC Goat Anti-Mouse (green) at 1:50 for 1 hour at RT.

sodium voltage-gated channel alpha subunit 9

sodium channel protein type 9 subunit alpha

Sodium channel protein type 9 subunit alpha

NENA; hNE-Na; PN1??[Similar Products]

SCN9A_HUMAN

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. [provided by RefSeq, Aug 2009]

SCN9A: Mediates the voltage-dependent sodium ion permeability of excitable membranes. Assuming opened or closed conformations in response to the voltage difference across the membrane, the protein forms a sodium-selective channel through which Na(+) ions may pass in accordance with their electrochemical gradient. It is a tetrodotoxin-sensitive Na(+) channel isoform. Plays a role in pain mechanisms, especially in the development of inflammatory pain. Defects in SCN9A are the cause of primary erythermalgia (PERYTHM). It is an autosomal dominant disease characterized by recurrent episodes of severe pain associated with redness and warmth in the feet or hands. Defects in SCN9A are the cause of congenital indifference to pain autosomal recessive (CIPAR); also known as channelopathy-associated insensitivity to pain. A disorder characterized by congenital inability to perceive any form of pain, in any part of the body. All other sensory modalities are preserved and the peripheral and central nervous systems are apparently intact. Patients perceive the sensations of touch, warm and cold temperature, proprioception, tickle and pressure, but not painful stimuli. There is no evidence of a motor or sensory neuropathy, either axonal or demyelinating. Defects in SCN9A are a cause of paroxysmal extreme pain disorder (PEPD); previously known as familial rectal pain (FRP). PEPD is an autosomal dominant paroxysmal disorder of pain and autonomic dysfunction. The distinctive features are paroxysmal episodes of burning pain in the rectal, ocular, and mandibular areas accompanied by autonomic manifestations such as skin flushing. Defects in SCN9A are a cause of generalized epilepsy with febrile seizures plus type 7 (GEFS+7). GEFS+7 is a rare autosomal dominant, familial condition with incomplete penetrance and large intrafamilial variability. Patients display febrile seizures persisting sometimes beyond the age of 6 years and/or a variety of afebrile seizure types. This disease combines febrile seizures, generalized seizures often precipitated by fever at age 6 years or more, and partial seizures, with a variable degree of severity. Defects in SCN9A are the cause of familial febrile convulsions type 3B (FEB3B). FEB3B consists of seizures associated with febrile episodes in childhood without any evidence of intracranial infection or defined pathologic or traumatic cause. It is a common condition, affecting 2-5% of children aged 3 months to 5 years. The majority are simple febrile seizures (generally defined as generalized onset, single seizures with a duration of less than 30 minutes). Complex febrile seizures are characterized by focal onset, duration greater than 30 minutes, and/or more than one seizure in a 24 hour period. The likelihood of developing epilepsy following simple febrile seizures is low. Complex febrile seizures are associated with a moderately increased incidence of epilepsy. Belongs to the sodium channel (TC 1.A.1.10) family. Nav1.7/SCN9A subfamily. 3 isoforms of the human protein are produced by alternative splicing.

Protein type: Membrane protein, integral; Channel, sodium; Membrane protein, multi-pass

Chromosomal Location of Human Ortholog: 2q24

Cellular Component: voltage-gated sodium channel complex; plasma membrane

Molecular Function: sodium ion binding; voltage-gated sodium channel activity

Biological Process: behavioral response to pain; response to toxin; sodium ion transport; generation of action potential; inflammatory response; post-embryonic development

Disease: Neuropathy, Hereditary Sensory And Autonomic, Type Iia; Generalized Epilepsy With Febrile Seizures Plus, Type 7; Erythermalgia, Primary; Paroxysmal Extreme Pain Disorder; Epileptic Encephalopathy, Early Infantile, 6; Indifference To Pain, Congenital, Autosomal Recessive

1. Dray A. (2008) Br. J. Anaesth. 101(1): 48-58. 2. Dray A., Read S.J (2007) Arthritis Res. Ther. 9(3): 212. 3. Samuels M.E., teMorshe R.H., Lynch M.E., Drenth J.P. (2008) Mol Pain. 4: 21.

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