Epithelial Sodium Channel, alpha, Rat (ENAC Alpha) Control Peptide

Produktübersicht

• Artikelname: Epithelial Sodium Channel, alpha, Rat (ENAC Alpha) Control Peptide
• Artikelnummer: USB-E3414-61F
• Hersteller Artikelnummer: E3414-61F
• Alternativnummer: USB-E3414-61F-100
• Hersteller: US Biological
• Kategorie: Molekularbiologie
• Applikation: ELISA, WB

Produktbeschreibung

A 20aa Peptide sequence near the N-terminus of rat ENACa (1) was selected for antibody production. The peptide was coupled to KLH. Tissue acidosis (decrease in pH below the physiological level) that occurs in ischemia, tissue damage or inflammation is accompanied by pain. At the molecular level, H+-gated cation channels are activated by low pH in nociceptive neurons. H+-gated cation channels, members of the NaC/DEG superfamily of Na channels that include amiloride-sensitive epithelial Na+ channel proteins (a, b, and g, and d-ENaC subunits), are expressed in epithelia of the vertebrate kidney, colon, lung, tongue, and brain. The ENaC subunits may form heterotrimeric active Na channel. ENaCs are involved in Na and water readsorption, and salty taste transduction) of vertebrate colon, lung, kidney and tongue. The superfamily of DEG/NaC proteins are characterized by intracellular N and C-termini, two TM domains, and a large extracellular loop. EN aC-alpha subunits have been cloned from various tissues and from several species (human 669 aa, rat 698 aa, mouse 699 aa, ~80% inter-species homology). It controls the reabsorption of Na in kidney, colon, lung, and sweat glands. ENaC-a has also been implicated in taste perception. Defects in ENaC-a are one of the cause of pseudohypoaldosteronism type I, a rare salt wasting disease characterized by dehydration, hyponatacemia, hyperkalemia, and acidosis. Inactivation of ENaC-a in transgenic mice causes an early death due to defective lung liquid clearance.

Produkteigenschaften

• Reinheit: Highly purified
• Formulierung: Supplied as a liquid in PBS, pH 7.2, 0.09% sodium azide