Thermo Fisher Scientific SCNN1B Polyclonal Antibody

Applications

Tested Dilution

Publications

Western Blot (WB)

1:500-1:2,000

-

Immunohistochemistry (Paraffin) (IHC (P))

1:50-1:200

-

Immunocytochemistry (ICC/IF)

1:100-1:500

-

Product Specifications

Species Reactivity

Human, Mouse, Rat

Host/Isotype

Rabbit / IgG

Class

Polyclonal

Type

Antibody

Immunogen

A synthesized peptide derived from human SCNN1B(Accession P51168), corresponding to amino acid residues N587-G637. if (typeof window.$mangular === undefined || !window.$mangular) { window.$mangular = {}; } $mangular.antigenJson = \[{targetFamily:SCNN1B,uniProtId:P51168-1,ncbiNodeId:9606,antigenRange:587-637,antigenLength:640,antigenImageFileName:PA5-106890_SCNN1B_P51168-1_Rabbit.svg,antigenImageFileNamePDP:PA5-106890_SCNN1B_P51168-1_Rabbit_PDP.jpeg,sortOrder:2}\]; $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_2854554

Product Specific Information

Antibody detects endogenous levels of total SCNN1B.

Target Information

Sodium permeable non-voltage-sensitive ion channel inhibited by the diuretic amiloride. Mediates the electrodiffusion of the luminal sodium (and water, which follows osmotically) through the apical membrane of epithelial cells. Controls the reabsorption of sodium in kidney, colon, lung and sweat glands. Also plays a role in taste perception. Heterotetramer of two alpha, one beta and one gamma subunit. A delta subunit can replace the alpha subunit. Interacts with the WW domains of NEDD4, NEDD4L, WWP1 and WWP2. Defects in SCNN1B are a cause of autosomal recessive pseudohypoaldosteronism type 1 (PHA1) [MIM:264350]. PHA1 is a rare salt wasting disease resulting from target organ unresponsiveness to mineralocorticoids. There are 2 forms of PHA1: the autosomal recessive form that is severe, and the dominant form which is more milder and due to defects in mineralocorticoid receptor. Autosomal recessive PHA1 is characterized by an often fulminant presentation in the neonatal period with dehydration, hyponatraemia, hyperkalaemia, metabolic acidosis, failure to thrive and weight loss. Defects in SCNN1B are a cause of Liddle syndrome. It is an autosomal dominant disorder characterized by pseudoaldosteronism and hypertension associated with hypokalemic alkalosis. The disease is caused by constitutive activation of the renal epithelial sodium channel.

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