Overview
Alomone Labs is pleased to offer the NaV1.8 Channel Premium Research Pack (#ESP-003). The Research Pack contains all you need for NaV1.8 research: Antibodies recognizing different domains of the channel and NaV1.8 blockers, all in one economical package!
Compounds
Product Name | Cat # | Size |
---|---|---|
Antibodies | ||
Anti-NaV1.8 (SCN10A) Antibody |
ASC-016 | 1 x 0.2 ml |
Nav1.8/SCN10A Blocking Peptide |
BLP-SC016 | 1 x 40 µg |
Guinea pig Anti-NaV1.8 (SCN10A) Antibody |
ASC-016-GP | 1 x 0.2 ml |
Nav1.8/SCN10A Blocking Peptide |
BLP-SC016 | 1 x 40 µg |
Anti-NaV1.8 (SCN10A) (extracellular) Antibody |
ASC-028 | 1 x 0.2 ml |
Nav1.8/SCN10A (extracellular) Blocking Peptide |
BLP-SC028 | 1 x 40 µg |
Blockers/Antagonists | ||
A-803467 |
A-105_50 mg | 1 x 50 mg |
VSTX3 |
STT-350 | 1 x 0.1 mg |
Scientific Background
Voltage-gated Na+ 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 NaV1.1-1.9. 2-3 The NaV channels are classified into two groups according to their sensitivity to tetrodotoxin (TTX): TTX-sensitive and TTX-resistant channels.4-5 Expression of the α subunit isoform is developmentally and tissue specific.
Two TTX-resistant NaV channels are expressed in dorsal root ganglion (DRG) neurons, NaV1.8 and NaV1.9. The NaV1.8 channel (also called SNS, SCN10A and PN3) is mainly expressed in small-diameter DRG neurons.4-6 TTX-resistant channels have been suggested to play an important role in nociceptive transmission.
Recently, involvement of NaV1.8 in multiple sclerosis (MS) was suggested due to up-regulation of both, mRNA and protein, in Purkinje cells of MS patients and also in animal models.6
- Lai, J. et al. (2003) Curr. Opin. Neurobiol. 13, 291.
- Renganathan, M. et al. (2003) Brain Res. 959, 235.
- Fang, X. et al. (2002) J. Neurosci. 22, 7425.
- Wu, L. et al. (2002) Neuro. Report 13, 2547.
- Baker, M.D. and Wood, J.N. (2001) Trends Pharmacol. Sci. 22, 27.
- Fjell, J. et al. (2000) Neuro. Report 11, 199.