Alomone Labs is pleased to offer the NaV1.7 Channel Deluxe Research Pack (#ESD-001). The Research Pack contains all you need for NaV1.7 research: Antibodies recognizing different domains of the channel, a classical NaV channel activator and NaV1.7 specific blockers, all in one economical package!
|Product Name||Cat #||Size|
|ASC-008||1 x 0.2 ml|
|ASC-008-FR||1 x 50 µl|
|AGP-057||1 x 0.2 ml|
|ASC-027||1 x 0.2 ml|
|N-310||1 x 10 mg|
|P-265||1 x 10 mg|
|STP-150||1 x 0.1 mg|
|P-275||1 x 10 mg|
|X-105||1 x 10 mg|
|STA-700||1 x 0.1 mg|
Voltage-gated sodium channels (NaV) are essential for the generation of action potentials and for cell excitability.1 NaV channels are activated in response to depolarization and selectively allow flow of Na+ ions. To date, nine Nav α subunits have been cloned and named NaV1.1-NaV1.9.4-5 The NaV channels are classified into two groups according to their sensitivity to Tetrodotoxin (TTX): TTX-sensitive (NaV1.1, NaV1.2, NaV1.3, NaV1.4, NaV1.6 and NaV1.7) and TTX-resistant (NaV1.5, NaV1.8 and NaV1.9).2-3 Mammalian sodium channels are heterotrimers, composed of a central, pore-forming α subunit and two auxiliary β subunits. Expression of the α subunit isoform is developmentally regulated and tissue specific. Sodium channels in the adult central nervous system and heart contain β1 through β4 subunits, whereas sodium channels in adult skeletal muscle have only the β1 subunit.6-8
NaV1.7 is predominantly expressed in dorsal root ganglions (DRG) of the peripheral nervous system. Dominant gain of function mutations in the NaV1.7 gene are associated with erythermalgia (a rare autosomal disease characterized by sporadic burning pain accompanied by redness and heat in the extremities).9-11 Loss, or function mutations in NaV1.7 channels, leads to complete ablation of pain perception in humans.11 These recent findings highlight the role of this NaV isoform and the subset of DRG neurons that express this channel in physiological pain sensation.
- Wu, L. et al. (2002) NeuroReport 13, 2547.
- Fang, X. et al. (2002) J. Neurosci. 22, 7425.
- Fjell, J. et al. (2000) NeuroReport 11, 199.
- Baker, M.D. and Wood, J.N. (2001) Trends Pharmacol. Sci. 22, 27.
- Lai, J. et al. (2003) Curr. Opin. Neurobiol. 13, 291.
- Isom, L.L. (2001) Neuroscientist 7, 42.
- Catterall, W.A. et al. (2003) Pharmacol Rev 55, 575.
- Catterall, W.A. et al. (2005) Pharmacol. Rev. 57, 397.
- Yang, Y. et al. (2004) J. Med. Genet. 41, 171.
- Cummins, T.R. et al. (2004) J. Neurosci. 24, 8232.
- Dray, A. (2008) Br. J. Anaesth. 101, 48.