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Nav1.8 Antibody
Nav1.8 Antibody, Clone S134-12
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, IHC, AM |
|---|---|
| Primary Accession | Q62968 |
| Other Accession | NP_058943.1 |
| Host | Mouse |
| Isotype | IgG2a |
| Reactivity | Human, Mouse, Rat, Monkey |
| Clonality | Monoclonal |
| Description | Mouse Anti-Rat Nav1.8 Monoclonal IgG2a |
| Target/Specificity | Detects ~220kDa. No cross reactivity against other Nav channels. |
| Other Names | mPN3 antibody, Peripheral nerve sodium channel 3 antibody, Pn3 (gene name) antibody, PN3 antibody, Scn10a antibody, Sensory neuron sodium channel antibody, Sns (gene name) antibody, SNS antibody, Sodium channel protein type 10 subunit alpha antibody, Sodium channel protein type X alpha subunit antibody, Voltage-gated sodium channel alpha subunit Nav1.8 antibody |
| Clone Names | S134-12 |
| Immunogen | Fusion protein amino acids 1724-1956 of rat Nav1.8 |
| Purification | Protein G Purified |
| Storage | -20ºC |
| Storage Buffer | PBS pH7.4, 50% glycerol, 0.09% sodium azide |
| Shipping Temperature | Blue Ice or 4ºC |
| Certificate of Analysis | 1 µg/ml of SMC-342 was sufficient for detection of Nav1.8 in 10 µg of COS cell lysate transiently expressing Nav1.8 by colorimetric immunoblot analysis using Goat anti-mouse IgG:HRP as the secondary antibody. |
| Cellular Localization | Membrane |
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Provided below are standard protocols that you may find useful for product applications.
Background
Nav1.8 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 Nav1.8 is not present in cardiac muscle or neurons in the central nervous system, blockers of Nav1.8 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.
References
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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