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Product Details
PEP-089
Product Specifications
Species Reactivity
Human
Class
Synthetic
Type
Peptide
Conjugate
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.
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Bioinformatics
Protein Aliases: Amiloride-sensitive sodium channel subunit beta; amiloride-sensitive sodium channel subunit beta 1; Beta ENaC; Beta-ENaC; Beta-NaCH; Epithelial Na(+) channel subunit beta; epithelial sodium channel beta-2 subunit; epithelial sodium channel beta-3 subunit; nasal epithelial sodium channel beta subunit; Nonvoltage-gated sodium channel 1 subunit beta; SCNEB; SCNN 1B; sodium channel, non voltage gated 1 beta subunit; sodium channel, non-voltage-gated 1, beta subunit; sodium channel, nonvoltage-gated 1, beta
Gene Aliases: BESC1; ENaCb; ENaCbeta; SCNEB; SCNN1B
UniProt ID: (Human) P51168
Entrez Gene ID: (Human) 6338
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