Render Target: STATIC
Render Timestamp: 2024-12-20T11:53:58.353Z
Commit: f2d32940205a64f990b886d724ccee2c9935daff
XML generation date: 2024-09-20 06:15:20.052
Product last modified at: 2024-09-10T20:30:11.255Z
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PDP - Template Name: Polyclonal Antibody
PDP - Template ID: *******59c6464

Nav1.7 Antibody #14573

Filter:
  • WB
  • IP

    Supporting Data

    REACTIVITY M R
    SENSITIVITY Endogenous
    MW (kDa) 230-250
    SOURCE Rabbit
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    Species Cross-Reactivity Key:
    • M-Mouse 
    • R-Rat 

    Product Information

    Product Usage Information

    Application Dilution
    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

    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 SCN9A gene are associated with primary erythermalgia, autosomal recessive congenital indifference to pain, and paroxysmal extreme pain disorder (13-15). Mutations in SCN9A 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).
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