SCNN1G
Reactivity: Human, Rat
IHC, ELISA
Host: Rabbit
Polyclonal
unconjugated
Application Notes
Immunohistochemistry on paraffin sections: 5 μg/mL. Western blot: 1 μg/mL. ELISA. Other applications not tested. Optimal dilutions are dependent on conditions and should be determined by the user.
Restrictions
For Research Use only
Concentration
0.5 mg/mL
Buffer
PBS containing 0.01 % Sodium Azide and 50 % Glycerol
Preservative
Sodium azide
Precaution of Use
This product contains sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
Handling Advice
Avoid repeated freezing and thawing.
Storage
4 °C/-20 °C
Storage Comment
Store undiluted at 2-8 °C for one month or (in aliquots) at-20 °C for longer.
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: Amiloride-sensitive sodium channel subunit gamma, ENaCG, Epithelial Na(+) channel subunit gamma, Gamma-ENaC, Gamma-NaCH, Nonvoltage-gated sodium channel 1 subunit gamma, SCNEG