Thermo Fisher Scientific alpha-ENaC Polyclonal Antibody

Applications

Tested Dilution

Publications

Immunohistochemistry (IHC)

1:300-1:2,000

-

Product Specifications

Host/Isotype

Rabbit / IgG

Class

Polyclonal

Type

Antibody

Immunogen

A synthetic peptide from the extracellular domain of human SCNN1A conjugated to an immunogenic carrier protein was used as the antigen.

Conjugate

Unconjugated Unconjugated Unconjugated

Form

Lyophilized

Concentration

Conc. Not Determined

Storage conditions

Store at 4°C short term. For long term storage, store at -20°C, avoiding freeze/thaw cycles. Glycerol (1:1) may be added for added stability.

Shipping conditions

Ambient (domestic); Wet ice (international)

RRID

AB_2184370

Product Specific Information

SCNN1 is highly expressed in kidney and lung tissues, detected at intermediate levels in pancreas and liver, and at low levels in heart and placenta.

Isoform 1 and isoform 2 are predominate in all tissues.

Expression of isoform 3, isoform 4 and isoform 5 are very low or not detectable, except in lung and heart tissues.

Target Information

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).

For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.