Thermo Fisher Scientific Human ENaC alpha (aa 20-42) Synthetic Peptide

Applications

Tested Dilution

Publications

Western Blot (WB)

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Control (Ctrl)

Assay-dependent

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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-088 is a 24 amino acid synthetic peptide whose sequence corresponds to residues 20-42 of human alpha-ENaC with a carboxy-terminal cysteine added for carrier protein conjugation. The sequence of this peptide is (amino to carboxy terminus): L (20)-M-K-G-N-K-R-E-E-Q-G-L-G-P-E-P-A-A-Q-Q-P-T (42)-C.

This peptide may be used for neutralization and control experiments with the polyclonal antibody that reacts with this product and endogenous alpha-ENaC, catalog # PA1-920A. 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

Epithelial sodium channels are amiloride-sensitive members of the degenerin/epithelial sodium channel (Deg/ENaC) superfamily of ion channels. Members of this superfamily of ion channels share organizational similarity in that they all possess two short intracellular amino and carboxyl termini, two short membrane spanning segments, and a large extracellular loop with a conserved cysteine-rich region. There are three homologous isoforms of the ENaC (alpha, beta, and gamma) protein. ENaC in the kidney, lung, and colon plays an essential role in trans-epithelial sodium and fluid balance. ENaC also mediates aldosterone-dependent sodium reabsorption in the distal nephron of the kidney, thus regulating blood pressure. ENaC is thought to be regulated, in part, through association with the cystic fibrosis transmembrane conductance regulator (CFTR) chloride ion channel. Gain-of-function mutations in beta- or gamma-ENaC can cause severe arterial hypertension (Liddel`s syndrome) and loss-of-function mutations in alpha- or beta-ENaC causes pseudohypoaldosteronism (PHA-1).

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