Na+ channel protein (pan) Rabbit Polyclonal Antibody

SKU AP06320PU-N

Na+ channel protein (pan) rabbit polyclonal antibody, Aff - Purified

Product Data

• Application: IF, IHC, WB
• Recommended Dilution: Western blot: 1/500-1/1000.; Immunohistochemistry on paraffin sections: 1/50-1/200.; Immunofluorescence: 1/50-1/200.
• Reactivity: Human, Mouse, Rat
• Antibody Host: Rabbit
• Clonality: Polyclonal
• Immunogen: Synthetic peptide, corresponding to amino acids 1470-1520 of Human SCN5A.
• Specificity: This antibody detects endogenous levels of Sodium Channel-pan protein.; (region surrounding Lys1493)
• Buffer: Phosphate buffered saline (PBS), pH~7.2; State: Aff - Purified; State: Liquid purified Ig fraction (> 95% pure by SDS-PAGE).; Preservative: 0.05% Sodium Azide
• Concentration: 1.0 mg/ml
• Purification: Affinity Chromatography using epitope-specific immunogen.
• Conjugation: Unconjugated
• Storage: Store undiluted at 2-8°C for one month or (in aliquots) at -20°C for longer.; Avoid repeated freezing and thawing.
• Stability: Shelf life: one year from despatch.
• Shipping: Blue Ice
• Predicted Protein Size: ~ 230 kDa
• Background: Epithelial sodium channels are amiloride-sensitive members of the Degenerin/epithelial sodium channel (Deg/ENaC) superfamily of ion channels. Members of this 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 (Liddel’s syndrome) and loss-of-function mutations in alpha- or beta-ENaC causes pseudohypoaldosteronism (PHA-1).
• Synonyms: Sodium channel protein pan

Reference Data