Thermo Fisher Scientific SCN1A Polyclonal Antibody

Applications

Tested Dilution

Publications

Western Blot (WB)

1:1,000-1:3,000

-

Product Specifications

Species Reactivity

Human, Mouse, Rat

Host/Isotype

Rabbit / IgG

Class

Polyclonal

Type

Antibody

Immunogen

Synthesized peptide derived from human SCN1A. if (typeof window.$mangular === undefined || !window.$mangular) { window.$mangular = {}; } $mangular.antigenJson = \[{targetFamily:SCN1A,uniProtId:P35498-1,ncbiNodeId:9606,antigenRange:456-482,antigenLength:2009,antigenImageFileName:PA5-67968_SCN1A_P35498-1_Rabbit.svg,antigenImageFileNamePDP:PA5-67968_SCN1A_P35498-1_Rabbit_PDP.jpeg,sortOrder:2}\]; $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

affinity chromatography

Storage buffer

PBS, pH 7.4, with 50% glycerol

Contains

0.02% sodium azide

Storage conditions

-20°C

Shipping conditions

Wet ice

RRID

AB_2691928

Product Specific Information

Predicted to react with Mouse and Rat samples.

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 (Liddels 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.