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anti-SCN9A antibody :: Mouse Nav1.7 Monoclonal Antibody

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Catalog # MBS804140
Unit / Price
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  0.1 mg  /  $390 +1 FREE 8GB USB
Product Name

Nav1.7 (SCN9A), Monoclonal Antibody

Full Product Name

Nav1.7 Antibody

Product Synonym Names
ETHA; hNE Na; NE NA; PN1; SCN9A; voltage gated sodium channel subunit alpha Nav1; peripheral sodium channel 1; neuroendocrine sodium channel
Matching Pairs
Unconjugated Antibody: Nav1.7 Clone #S68-6 (MBS804140)
Alkaline Phosphatase Conjugated Antibody: Nav1.7 Clone #S68-6 (MBS800252)
Matching Pairs
Unconjugated Antibody: Nav1.7 Clone #S68-6 (MBS804140)
PerCP Conjugated Antibody: Nav1.7 Clone #S68-6 (MBS801415)
Matching Pairs
Unconjugated Antibody: Nav1.7 Clone #S68-6 (MBS804140)
HRP Conjugated Antibody: Nav1.7 Clone #S68-6 (MBS801586)
Research Use Only
For Research Use Only. Not for use in diagnostic procedures.
OMIM
gene 613863
3D Structure
ModBase 3D Structure for Q15858
Clonality
Monoclonal
Isotype
IgG1
Clone Number
S68-6
Host
Mouse
Species Reactivity
Human, Mouse, Rat
Form/Format
Protein G Purified
Concentration
1mg/mL (lot specific)
Certificate of Analysis
1 ug/mL was sufficient for detection of Nav1.7 in 10ug of HEK-293 cell lysate transiently expressing Nav1.7 by colorimetric immunoblot analysis using Goat anti-mouse IgG:HRP as the secondary antibody.
Storage Buffer
PBS pH7.4, 50% glycerol, 0.09% sodium azide
Preparation and Storage
-20 degree C
Other Notes
Small volumes of anti-SCN9A 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.
Related Product Information for
anti-SCN9A antibody
Background Info: Detects ~230kDa. No cross-reactivity against other Nav channels.

Scientific Background: Ion channels are integral membrane proteins that help establish and control the small voltage gradient across the plasma membrane of living cells by allowing the flow of ions down their electrochemical gradient (1). They are present in the membranes that surround all biological cells because their main function is to regulate the flow of ions across this membrane. Whereas some ion channels permit the passage of ions based on charge, others conduct based on a ionic species, such as sodium or potassium. Furthermore, in some ion channels, the passage is governed by a gate which is controlled by chemical or electrical signals, temperature, or mechanical forces. There are a few main classifications of gated ion channels. There are voltage- gated ion channels, ligand- gated, other gating systems and finally those that are classified differently, having more exotic characteristics. The first are voltage- gated ion channels which open and close in response to membrane potential. These are then separated into sodium, calcium, potassium, proton, transient receptor, and cyclic nucleotide-gated channels; each of which is responsible for a unique role. Ligand-gated ion channels are also known as ionotropic receptors, and they open in response to specific ligand molecules binding to the extracellular domain of the receptor protein. The other gated classifications include activation and inactivation by second messengers, inward-rectifier potassium channels, calcium-activated potassium channels, two-pore-domain potassium channels, light-gated channels, mechano-sensitive ion channels and cyclic nucleotide-gated channels. Finally, the other classifications are based on less normal characteristics such as two-pore channels, and transient receptor potential channels (2). 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 (3-5).
Product Categories/Family for anti-SCN9A antibody
Applications Tested/Suitable for anti-SCN9A antibody
Western Blot (WB), Immunoprecipitation (IP), Immunocytochemistry (ICC), Immunofluorescence (IF)
Application Notes for anti-SCN9A antibody
1-10ug/mL (WB), 0.1-1.0ug/mL (Perox) (IHC/ICC), 1.0-10ug/mL (IF)

Immunohistochemistry (IHC) of anti-SCN9A antibody
Immunohistochemistry analysis using Mouse Anti-Nav1.7 Sodium Channel Monoclonal Antibody, Clone S68-6. Tissue: Brain Slice. Species: Mouse. Fixation: Frozen sections. Primary Antibody: Mouse Anti-Nav1.7 Sodium Channel Monoclonal Antibody 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.
anti-SCN9A antibody Immunohistochemistry (IHC) (IHC) image
Western Blot (WB) of anti-SCN9A antibody
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. Load: 15 ug. Block: 1.5% BSA for 30 minutes at RT. Primary Antibody: Mouse Anti-Nav1.7 Sodium Channel Monoclonal Antibody at 1:1000 for 2 hours at RT. Secondary Antibody: Sheep Anti-Mouse IgG: HRP for 1 hour at RT.
anti-SCN9A antibody Western Blot (WB) (WB) image
Immunohistochemistry (IHC) of anti-SCN9A antibody
Immunohistochemistry analysis using Mouse Anti-Nav1.7 Sodium Channel Monoclonal Antibody, Clone S68-6. Tissue: hippocampus. Species: Human. Fixation: Bouin's Fixative and paraffin-embedded. Primary Antibody: Mouse Anti-Nav1.7 Sodium Channel Monoclonal Antibody at 1:1000 for 1 hour at RT. Secondary Antibody: FITC Goat Anti-Mouse (green) at 1:50 for 1 hour at RT.
anti-SCN9A antibody Immunohistochemistry (IHC) (IHC) image
Immunohistochemistry (IHC) of anti-SCN9A antibody
Immunohistochemistry analysis using Mouse Anti-Nav1.7 Sodium Channel Monoclonal Antibody, Clone S68-6. Tissue: backskin. Species: Mouse. Fixation: Bouin's Fixative and paraffin-embedded. Primary Antibody: Mouse Anti-Nav1.7 Sodium Channel Monoclonal Antibody at 1:100 for 1 hour at RT. Secondary Antibody: FITC Goat Anti-Mouse (green) at 1:50 for 1 hour at RT.
anti-SCN9A antibody Immunohistochemistry (IHC) (IHC) image
NCBI/Uniprot data below describe general gene information for SCN9A. It may not necessarily be applicable to this product.
NCBI GI #
NCBI GeneID
NCBI Accession #
NCBI GenBank Nucleotide #
UniProt Primary Accession #
UniProt Secondary Accession #
UniProt Related Accession #
Molecular Weight
225,227 Da[Similar Products]
NCBI Official Full Name
sodium channel protein type 9 subunit alpha
NCBI Official Synonym Full Names
sodium channel, voltage-gated, type IX, alpha subunit
NCBI Official Symbol
SCN9A  [Similar Products]
NCBI Official Synonym Symbols
PN1; ETHA; NENA; SFNP; FEB3B; NE-NA; GEFSP7; Nav1.7
  [Similar Products]
NCBI Protein Information
sodium channel protein type 9 subunit alpha; hNE-Na; peripheral sodium channel 1; neuroendocrine sodium channel; sodium channel protein type IX subunit alpha; voltage-gated sodium channel alpha subunit Nav1.7; voltage-gated sodium channel subunit alpha Nav1.7; sodium channel, voltage-gated, type IX, alpha polypeptide
UniProt Protein Name
Sodium channel protein type 9 subunit alpha
UniProt Synonym Protein Names
Neuroendocrine sodium channel; hNE-Na; Peripheral sodium channel 1; PN1; Sodium channel protein type IX subunit alpha; Voltage-gated sodium channel subunit alpha Nav1.7
Protein Family
UniProt Gene Name
SCN9A  [Similar Products]
UniProt Synonym Gene Names
NENA; hNE-Na; PN1  [Similar Products]
UniProt Entry Name
SCN9A_HUMAN
NCBI Summary for SCN9A
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]
UniProt Comments for SCN9A
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: Channel, sodium; Membrane protein, integral; 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
Product References and Citations for anti-SCN9A antibody
1. Hille B. (2001) Ion Channels of Excitable Membranes, 3rd Ed., Sinauer Associated Inc.: Sunderland, MA USA. 2. www.iochannels.org 3. Dray A. (2008) Br. J. Anaesth. 101(1): 48-58. 4. Dray A., Read S.J (2007) Arthritis Res. Ther. 9(3): 212. 5. Samuels M.E., teMorshe R.H., Lynch M.E., Drenth J.P. (2008) Mol Pain. 4: 21.

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