An antibody raised against SCN9A/Nav1.7, a protein that encodes a specific alpha subunit of sodium channels expressed predominantly in nociceptors.
Catalogue number crb2005679 Disease Area Primary Erythermalgia (PERYTHM), CIP, Paroxysmal Extreme Pain Disorder (PEPD) Antibody Anti-SCN9A/Nav1.7 antibody Antigen Peptide KLH conjugated synthetic peptide crb1200888 Protein ID UniProtKB - Q15858 Aliases Sodium channel protein type 9 subunit alpha, Neuroendocrine sodium channel (hNE-Na), Peripheral sodium channel, NENA SCN9A, Voltage-gated sodium channel subunit alpha Nav1.7 Sodium channel protein type IX subunit alpha, 1 (PN1) Cross-Reactivity Human Host Species Rabbit Antibody Type Polyclonal Concentration 0.5 mg/ml Glycine (R1G), 0.2 mg/ml TEA (R1T), 0.5 mg/ml Glycine (R2G), 0.2 mg/ml TEA (R2T) Target SCN9A/Nav1.7 Family Sodium channel (TC 1.A.1.10) family. Nav1.7/SCN9A subfamily Storage This material is supplied in PBS containing 0.01% sodium azide and 1% trehalose. The product should be stored at +4°C for short term storage and -20°C for long term storage. Avoid repeated freeze/thaw cycles. References
Yang et al. (2004). Mutations in SCN9A, Encoding a Sodium Channel Alpha Subunit, in Patients with Primary Erythermalgia. Journal of Medical Genetics. 41(3):171-174
Eagles et al. (2020) Fifteen Years of Nav1.7 Channels as an Analgesic Target: Why has Excellent In Vitro Pharmacology Not Translated into In Vivo Analgesic Efficacy? British Journal of Pharmacology. 179(14):3592-3611
Neff et al. (2021) Selective Targeting of Nav1.7 with Engineered Spider Venom-Based Peptides. National Library of Medicine. 15(1):179-193
Sodium channel protein type 9 subunit alpha gene, SCN9A, is responsible for regulation of Na+ ion permeability across excitable membranes. Found on chromosome 2, SCN9A mediates the passage of Na+ ions through the formation of an alpha subunit, known as Nav1.7, in voltage-gated sodium channels primarily expressed in neurones belonging to the peripheral nervous system.
Sodium channels synthesised under the action of SCN9A originate from the Degenerin/epithelial (Deg/ENaC) ion channel superfamily that share common organisational features including an extracellular loop accompanied by a conserved cysteine-rich region, two membrane-spanning segments and two intracellular carboxyl and amino termini. Members of this family, and their respective alpha, beta and gamma isoforms, are associated with maintaining transepithelial sodium balance in the kidneys, lungs and colon.
The widespread expression of Nav1.7 at peripheral terminals of intraepidermal nerve fibres makes them a likely contributor to axonal conduction and presynaptic neurotransmitter release in nociceptors. Loss-of-function mutations in SNC9A have been linked to congenital insensitivity to pain (CIP) and anosmia in humans.