CST, 14573S, Nav1.7 Antibody

Polyclonal Antibody for studying SCN9A. Validated for Western Blotting,Immunoprecipitation. Highly specific and rigorously validated in-house, Nav1.7 Antibody (CST #14573) is ready to ship. Product Usage Information Western Blotting: 1:1000 Immunoprecipitation: 1:50 Storage Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA and 50% glycerol. Store at -20°C. Do not aliquot the antibody. Protocol Available protocols: Western Blotting, Immunoprecipitation Specificity / Sensitivity Nav1.7 Antibody recognizes endogenous levels of total Nav1.7 protein. Species Reactivity: Mouse, Rat Source / Purification Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy terminus of human Nav1.7 protein. Antibodies are purified by protein A and peptide affinity chromatography. Background Voltage gated sodium channels are composed of a large alpha subunit and auxiliary beta subunits. The alpha subunit has 4 homologous domains, with each domain containing 6 transmembrane segments. These segments function as the voltage sensor and sodium permeable pore. Upon change of membrane potential, the sodium channel is activated, which allows sodium ions to flow through (1,2). When associated with beta subunits or other accessory proteins, the alpha subunit is regulated at the level of cell surface expression, kinetics, and voltage dependence (3,4). 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 gene are associated with primary erythermalgia, autosomal recessive congenital indifference to pain, and paroxysmal extreme pain disorder (13-15). Mutations in 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). 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 Specification REACTIVITY: M R SENSITIVITY: Endogenous MW (kDa): 230-250 SOURCE: Rabbit