产品描述： 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).