Nav1.7 (D5L1J) Rabbit Monoclonal Antibody (BSA and Azide Free) #81929
- WB
Product Specifications
| REACTIVITY | H M R |
| SENSITIVITY | Endogenous |
| MW (kDa) | 250 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
- R-Rat
Product Information
Product Usage Information
This formulation is ideal for use with technologies requiring specialized or custom antibody labeling, including fluorophores, metals, lanthanides, and oligonucleotides. It is not recommended for ChIP, ChIP-seq, CUT&RUN or CUT&Tag assays. If you require a carrier free formulation for chromatin profiling, please contact us. Optimal dilutions/concentrations should be determined by the end user.
BSA and Azide Free antibodies are quality control tested by size exclusion chromatography (SEC) to determine antibody integrity.
Formulation
For standard formulation of this product see product #78889
Storage
Specificity / Sensitivity
Species Reactivity:
Source / Purification
Background
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.
Alternate Names
ETHA; FEB3B; GEFSP7; hNE-Na; HSAN2D; Nav1.7; NE-NA; NENA; Neuroendocrine sodium channel; Peripheral sodium channel 1; PN1; SCN9A; SFNP; Sodium channel protein type 9 subunit alpha; Sodium channel protein type IX subunit alpha; sodium channel, voltage-gated, type IX, alpha polypeptide; sodium channel, voltage-gated, type IX, alpha subunit; sodium voltage-gated channel alpha subunit 9; voltage-gated sodium channel alpha subunit Nav1.7; Voltage-gated sodium channel subunit alpha Nav1.7
Limited Uses
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