Thermo Fisher Scientific SCNN1G Polyclonal Antibody

Applications

Tested Dilution

Publications

Western Blot (WB)

1:500-1:2,000

-

Product Specifications

Species Reactivity

Human, Mouse, Rat

Host/Isotype

Rabbit / IgG

Class

Polyclonal

Type

Antibody

Immunogen

Synthesized peptide derived from the Internal region of human ENaC ENaC G. if (typeof window.$mangular === undefined || !window.$mangular) { window.$mangular = {}; } $mangular.antigenJson = \[{targetFamily:SCNN1G,uniProtId:P51170-1,ncbiNodeId:9606,antigenRange:621-647,antigenLength:649,antigenImageFileName:PA5-51073_SCNN1G_P51170-1_Rabbit.svg,antigenImageFileNamePDP:PA5-51073_SCNN1G_P51170-1_Rabbit_PDP.jpeg,sortOrder:1}\]; $mangular.isB2BCMGT = false; $mangular.isEpitopesModalImageMultiSizeEnabled = true;

View immunogen .st0{fill:#FFFFFF;} .st1{fill:#1E8AE7;}

Conjugate

Unconjugated Unconjugated Unconjugated

Form

Liquid

Concentration

1 mg/mL

Purification

Antigen affinity chromatography

Storage buffer

PBS, pH 7.4, with 50% glycerol, 0.5% BSA

Contains

0.02% sodium azide

Storage conditions

-20° C, Avoid Freeze/Thaw Cycles

Shipping conditions

Ambient (domestic); Wet ice (international)

RRID

AB_2636521

Product Specific Information

SCNN1G Polyclonal Antibody detects endogenous levels of SCNN1G protein.

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.