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SCNN1B Rabbit anti-Human, Polyclonal, Invitrogen™

Rabbit Polyclonal Antibody

Manufacturer:  Invitrogen OSR00125W

Catalog No. PIOSR00125W

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Glycerol (1:1) may be added for additional stability.

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 domit form which is more milder and due to defects in mineralocorticoid receptor. Autosomal recessive PHA1 is characterized by an often fulmit 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 domit disorder characterized by pseudoaldosteronism and hypertension associated with hypokalemic alkalosis. The disease is caused by constitutive activation of the renal epithelial sodium channel.


whole serum with no preservative
Beta-ENaC, Nonvoltage-gated sodium channel 1 subunit beta, SCNEB, Beta-NaCH, ENaCB, ENaCbeta
Immunohistochemistry, Western Blot
A synthetic peptide from aa region 570-640 of human SCNN1B conjugated to an immunogenic carrier protein was used as the antigen
100 μL
Store at 4°C short term. For long term storage, store at -20°C, avoiding freeze/thaw cycles.
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