SCN10A Monoclonal Antibody (S134), FITC, Invitrogen™

Description

• 1 μg/mL of MA5-45470 was sufficient for detection of Nav1.8 in 10 μg of COS cell lysate transiently expressing Nav1.8 by colorimetric immunoblot analysis using Goat anti-mouse IgG:HRP as the secondary antibody.∣Detects approximately 220kDa
• No cross reactivity against other Nav channels
• Scn10a is a tetrodotoxin-resistant voltage-gated sodium channel alpha subunit
• Epithelial sodium channels are amiloride-sensitive members of the Degenerin/epithelial sodium channel (Deg/ENaC) superfamily of ion channels
• Scn10a mediates the voltage-dependent sodium ion permeability of excitable membranes
• Assuming opened or closed conformations in response to the voltage difference across the membrane, Scn10a forms a sodium-selective channel through which sodium ions may pass in accordance with their electrochemical gradient
• Scn10a also plays a role in neuropathic pain mechanisms
• Structurally, members of Deg/ENaC superfamily of ion channels share organizational similarity in that they all possess two short intracellular amino and carboxyl termini, two short membrane spanning segments, and a large extracellular loop with a conserved cysteine-rich region
• There are three homologous isoforms of the ENaC (alpha, beta, and gamma) protein
• ENaC in the kidney, lung, and colon plays an essential role in trans-epithelial sodium and fluid balance
• ENaC also mediates aldosterone-dependent sodium reabsorption in the distal nephron of the kidney, thus regulating blood pressure
• ENaC is thought to be regulated, in part, through association with the cystic fibrosis transmembrane conductance regulator (CFTR) chloride ion channel
• Gain-of-function mutations in beta- or gamma-ENaC can cause severe arterial hypertension (Liddels syndrome) and loss-of-function mutations in alpha- or beta-ENaC causes pseudohypoaldosteronism (PHA-1)
• Diseases associated with SCN10A include Episodic Pain Syndrome, Familial, 2 and Sodium Channelopathy-Related Small Fiber Neuropathy.