Technical Data
Sodium channel Nav1.7
Voltage-gated sodium channel subunit alpha Nav1.7 (Nav1.7) is a multi-pass membrane protein containing a single IQ domain that belongs to the sodium channel family. NAV1.7 localizes to the terminal ends of sensory neurons and is believed to have a role in inflammatory pain development and mechanisms. It serves to regulate excitable membrane voltage-dependent Na+ ion permeability. There is a strong probability that Nav1.7 is involved in the transmission of nociceptive information, a suggested involvement supported by its role in a variety of chronic pain neuropathies induced by damage to the peripheral nerves. Nav1.7 is predominantly observed in dorsal root ganglion, and sensory and sympathetic neurons. Lower levels of the protein have been observed in MTC cell line, C-cell carcinoma, and smooth muscle cells. Defects in Nav1.7 expression are causal to several diseases such as autosomal recessive congenital indifference pain, primary erythermalgia, and paroxysmal extreme pain disorder or PEPD.

Suitable for use in Western Blot and Immunohistochemistry. Other applications have not been tested.

Recommended Dilutions:
Immunohistochemistry: 1:400 detects Nav1.7 in rat cerebellum tissue.
Optimal dilutions to be determined by the researcher.

Positive Control:
Rat cerebellum tissue

Storage and Stability:
May be stored at 4C for short-term only. Aliquot to avoid repeated freezing and thawing. Store at -20C. Aliquots are stable for 12 months after receipt. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap.

MabIgG1,k11C247Affinity Purified
100ug-20CBlue IceHumanMouse
Recombinant protein corresponding to human Nav1.7.
Purified by Protein G affinity chromatography.
Supplied as a liquid in 0.1M Tris-Glycine, pH 7.4, 150 mM sodium chloride, 0.05% sodium azide.
Recognizes human Sodium channel Nav1.7. Species crossreactivity: rat
Intended for research use only. Not for use in human, therapeutic, or diagnostic applications.
1. Maertens, C., et al. (2006). Molecular Pharmacology. 70(1):405-414. 2. Michaels, J.J., et al. (2005). Arch Neurol. 62: 1587-1590.