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  • alpha-ENaC Proteins

Invitrogen

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

View all (2) alpha-ENaC proteins

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

Product Details

RP-90101

Applications
Tested Dilution
Publications

Control (Ctrl)

Assay-dependent
-

Blocking Assay (BLOCK)

Assay-dependent
-
Product Specifications

Species

Human

Expression System

E. coli

Amino acid sequence

RYPEIKEELEELDRITEQTLFDLYKYSSFTTLVAGSRSRRDLRGTLPHPLQRLRVPPPPHGARRARSVASSLRDNNPQVDWKDWKIGFQL

Tag

His-ABP-tag

Class

Recombinant

Type

Protein

Purity

>80% by SDS-PAGE and Coomassie blue staining

Conjugate

Unconjugated Unconjugated Unconjugated

Form

Liquid

Concentration

≥5.0 mg/mL

Purification

purified

Storage buffer

1M urea/PBS, pH 7.4

Contains

no preservative

Storage conditions

-20°C, Avoid Freeze/Thaw Cycles

Product Specific Information

Highest antigen sequence indentity to the following orthologs: Mouse (78%), Rat (78%).

This recombinant protein control fragment may be used for blocking experiments. In IHC/ICC and WB experiments, we recommend a 100x molar excess of the protein fragment control based on the concentration and the molecular weight. Pre-incubate the antibody-protein control fragment mixture for 30 min at room temperature.

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.

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Bioinformatics

Protein Aliases: alpha ENaC-2; Alpha-ENaC; Alpha-NaCH; amiloride-sensitive epithelial sodium channel alpha subunit; Amiloride-sensitive sodium channel subunit alpha; amiloride-sensitive sodium channel subunit alpha 2; epithelial Na(+) channel subunit alpha; Epithelial sodium channel subunit alpha; FLJ21883; nasal epithelial sodium channel alpha subunit; Nonvoltage-gated sodium channel 1 subunit alpha; SCNEA; Sodium channel epithelial 1 subunit alpha; sodium channel, non voltage gated 1 alpha subunit; sodium channel, non-voltage-gated 1 alpha subunit; sodium channel, nonvoltage-gated 1 alpha

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Gene Aliases: BESC2; ENaCa; ENaCalpha; SCNEA; SCNN1; SCNN1A

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UniProt ID: (Human) P37088

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Entrez Gene ID: (Human) 6337

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It has to be done as per old AB suggested Products section.
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