Human alpha-ENaC (aa 139-228) Control Fragment Recombinant Protein

This webpage contains legacy information. The product is either no longer available from the supplier or has been delisted at Labome.

product summary

company name :

Invitrogen

other brands :

NeoMarkers, Lab Vision, Endogen, Pierce, BioSource International, Zymed Laboratories, Caltag, Molecular Probes, Research Genetics, Life Technologies, Applied Biosystems, GIBCO BRL, ABgene, Dynal, Affinity BioReagents, Nunc, Invitrogen, NatuTec, Oxoid, Richard-Allan Scientific, Arcturus, Perseptive Biosystems, Proxeon, eBioscience

product type :

protein

product name :

Human alpha-ENaC (aa 139-228) Control Fragment Recombinant Protein

catalog :

RP-90101

quantity :

100 uL

price :

US 259.00

product information

Product Type :

Protein

Product Name :

Human alpha-ENaC (aa 139-228) Control Fragment Recombinant Protein

Catalog # :

RP-90101

Quantity :

100 uL

Price :

US 259.00

Clonality :

Recombinant

Purity :

purified

Reactivity :

Human

Applications :

Blocking Assay: Assay-dependent, Control: Assay-dependent

Species :

Human

Storage :

-20 C, Avoid Freeze/Thaw Cycles

Description :

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).

Format :

Liquid

Applications w/Dilutions :

Blocking Assay: Assay-dependent, Control: Assay-dependent

Aliases :

alpha ENaC-2; alpha-ENaC; Alpha-NaCH; amiloride-sensitive epithelial sodium channel; amiloride-sensitive epithelial sodium channel alpha subunit; amiloride-sensitive sodium channel subunit alpha; amiloride-sensitive sodium channel subunit alpha 2; BESC2; ENaC; ENaC alpha; ENaCa; ENaCalpha; Epithelial Na(+) channel subunit alpha; epithelial sodium channel alpha subunit; FLJ21883; mENaC; nasal epithelial sodium channel alpha subunit; nonvoltage-gated sodium channel 1 subunit alpha; Renac; SCNEA; SCNN1; Scnn1a; sodium channel epithelial 1 alpha subunit; sodium channel, non voltage gated 1 alpha subunit; sodium channel, nonvoltage-gated 1 alpha; sodium channel, non-voltage-gated 1 alpha subunit; sodium channel, nonvoltage-gated, type I, alpha; sodium channel, nonvoltage-gated, type I, alpha polypeptide