NaV1.2 Channel Basic Research Pack

All You Need for NaV1.2 Channel Research
  • Lyophilized Powder
  • Antigen Incl.
  • Bioassay Tested
  • Shipped at Room Temp.
  • 100% Net Peptide
Cat #: ESB-002
Sizes: 6 Vials
Last update: 02/09/2018

Alomone Labs is pleased to offer the NaV1.2 Channel Basic Research Pack (#ESB-002). The Research Pack contains all you need for NaV1.2 research: An antibody specifically recognizing NaV1.2, classical NaV channel activators and NaV1.2 blockers, all in one economical package!

For research purposes only, not for human use
Compounds
Product NameCat #Size
Anti-SCN2A (NaV1.2) Antibody
ASC-002 1 x 0.2 ml
ATX-II
STA-700 1 x 0.1 mg
Lamotrigine
L-205 1 x 250 mg
α-Pompilidotoxin
P-170 1 x 10 mg
QX-314 chloride
Q-150 1 x 100 mg
Scientific Background
Scientific Background

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. The 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.6,7

Nav1.2 is primarily expressed in the central nervous system (CNS) and is localized in unmyelinated or premyelinated axons and dendrites. Mutations in the Nav1.2 channel have been identified in different types of epilepsy.

References
  1. Wu, L. et al. (2002) NeuroReport 13, 2547.
  2. Fang, Xet al. (2002) J. Neurosci22, 7425.
  3. Fjell, Jet al. (2000) NeuroReport 11, 199.
  4. Baker, M.D. and Wood, J.N. (2001) Trends Pharmacol. Sci. 22, 27.
  5. Lai, J. et al. (2003) Curr. Opin. Neurobiol. 13, 291.
  6. Isom, L.L. (2001) Neuroscientist 7, 42.
  7. Catterall, W.Aet al. (2003) Pharmacol. Rev. 55, 579.
  8. Catterall, W.A. et al. (2008) J. Neurosci28, 11768.
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