Thermo Fisher Scientific Human SCNN1B (aa 619-640) Synthetic Peptide

Applications

Tested Dilution

Publications

Control (Ctrl)

Assay-dependent

-

Product Specifications

Species Reactivity

Human

Class

Synthetic

Type

Peptide

Conjugate

Unconjugated Unconjugated Unconjugated

Form

Lyophilized

Concentration

0.5 mg/mL

Purification

purified

Contains

no preservative

Storage conditions

-20° C, Avoid Freeze/Thaw Cycles

Shipping conditions

Wet ice

Product Specific Information

PEP-089 is a 23 amino acid synthetic peptide whose sequence corresponds to amino acids 619-640 of the human beta-ENaC with an N-terminal cysteine added for carrier protein conjugation. The sequence of this peptide is (amino to carboxy terminus): C N (619)-Y-D-S-L-R-L-Q-P-L-D-V-I-E-S-D-S-E-G-D-A-I (640)

This peptide may be used for neutralization and control experiments with the polyclonal antibody that reacts with this product and human beta-ENaC, catalog # PA1-921. Using a solution of peptide of equal volume and concentration to the corresponding antibody will yield a large molar excess of peptide (~70-fold) for competitive inhibition of antibody-protein binding reactions.

Reconstitute with 0.1 mL of distilled water.

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.