WB, IP
M R
Endogenous
230-250
Rabbit
#Q15858
6335
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Immunoprecipitation | 1:50 |
Storage
Specificity / Sensitivity
Species Reactivity:
Mouse, Rat
Source / Purification
Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy terminus of human Nav1.7 protein. Antibodies are purified by protein A and peptide affinity chromatography.
Background
Voltage gated sodium channels are composed of a large alpha subunit and auxiliary beta subunits. The alpha subunit has 4 homologous domains, with each domain containing 6 transmembrane segments. These segments function as the voltage sensor and sodium permeable pore. Upon change of membrane potential, the sodium channel is activated, which allows sodium ions to flow through (1,2). When associated with beta subunits or other accessory proteins, the alpha subunit is regulated at the level of cell surface expression, kinetics, and voltage dependence (3,4).
There are 9 mammalian alpha subunits, named Nav1.1-Nav1.9 (5). These alpha subunits differ in tissue specificity and biophysical functions (6,7). Seven of these subunits are essential for the initiation and propagation of action potentials in the central and peripheral nervous system while Nav1.4 and Nav1.5 are mainly expressed in skeletal muscle and cardiac muscle (8,9). Mutations in these alpha channel subunits have been identified in patients with epilepsy, seizure, ataxia, sensitivity to pain, and cardiomyopathy (reviewed in 10).
The Nav1.7 alpha subunit (Nav1.7, SCN9A) plays an important role in nociception signaling and is essential for acute, inflammatory, and neuropathic pain perception (11,12). Mutations in the corresponding SCN9A gene are associated with primary erythermalgia, autosomal recessive congenital indifference to pain, and paroxysmal extreme pain disorder (13-15). Mutations in SCN9A cause the GEFSP7 form of generalized epilepsy with febrile seizures, and are implicated in many cases of Dravet syndrome, a severe form of pediatric epileptic encephalopathy (16).
- Catterall, W.A. (2000) Neuron 26, 13-25.
- Yu, F.H. and Catterall, W.A. (2003) Genome Biol 4, 207.
- Isom, L.L. et al. (1994) Neuron 12, 1183-94.
- Yu, F.H. et al. (2003) J Neurosci 23, 7577-85.
- Goldin, A.L. et al. (2000) Neuron 28, 365-8.
- Plummer, N.W. and Meisler, M.H. (1999) Genomics 57, 323-31.
- Goldin, A.L. (2001) Annu Rev Physiol 63, 871-94.
- George, A.L. et al. (1992) Ann Neurol 31, 131-7.
- Ou, Y. et al. (2002) Neurogastroenterol Motil 14, 477-86.
- Meisler, M.H. and Kearney, J.A. (2005) J Clin Invest 115, 2010-7.
- Minett, M.S. et al. (2012) Nat Commun 3, 791.
- Minett, M.S. et al. (2014) PLoS One 9, e104458.
- Yang, Y. et al. (2004) J Med Genet 41, 171-4.
- Cox, J.J. et al. (2010) Hum Mutat 31, E1670-86.
- Fertleman, C.R. et al. (2006) Neuron 52, 767-74.
- Mulley, J.C. et al. (2013) Epilepsia 54, e122-6.
Species Reactivity
Species reactivity is determined by testing in at least one approved application (e.g., western blot).
Western Blot Buffer
IMPORTANT: For western blots, incubate membrane with diluted primary antibody in 5% w/v BSA, 1X TBS, 0.1% Tween® 20 at 4°C with gentle shaking, overnight.
Applications Key
WB: Western Blotting IP: Immunoprecipitation
Cross-Reactivity Key
H: human M: mouse R: rat Hm: hamster Mk: monkey Vir: virus Mi: mink C: chicken Dm: D. melanogaster X: Xenopus Z: zebrafish B: bovine Dg: dog Pg: pig Sc: S. cerevisiae Ce: C. elegans Hr: horse GP: Guinea Pig Rab: rabbit All: all species expected
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