Thermo Fisher Scientific SCNN1B Polyclonal Antibody

Applications

Tested Dilution

Publications

Western Blot (WB)

1:300-1:2,000

-

Immunohistochemistry (IHC)

1:300-1:2,000

-

Miscellaneous PubMed (Misc)

-

View 1 publication 1 publication

Product Specifications

Species Reactivity

Human

Published species

Not Applicable

Host/Isotype

Rabbit / Ig

Class

Polyclonal

Type

Antibody

Immunogen

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Conjugate

Unconjugated Unconjugated Unconjugated

Form

Lyophilized

Concentration

Conc. Not Determined

Storage buffer

whole serum

Contains

no preservative

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)

Product Specific Information

Reconstitute in 100 µL of sterile water. Centrifuge to remove any insoluble material.

Specificity of this antibody: 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.