| Details | |
| Host / Isotype: | Rabbit / IgG |
| Class: | Polyclonal |
| Type: | Antibody |
| Species Reactivity: | Rat (Rt) |
| Immunogen: | Synthetic peptide corresponding to residues N(619) Y D S L R L Q P L D V I E S D S E G D A I(640) of rat beta-ENaC |
| Ordering Information | ||||
| Pierce beta ENaC Antibody |
| Storage: | -20° C, Avoid Freeze/Thaw Cycles |
| Form: | 100 µg of epitope affinity purified IgG (1 mg/ml) in PBS containing 1 mg/ml BSA and 0.05% sodium azide. |
| Applications | Dilution * |
| Immunoprecipitation (IP) | Assay dependent |
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* Suggested working dilutions are given as a guide only. It is recommended that the user titrates the product for use in their own experiment using appropriate negative and positive controls.
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| Product Specific Information |
| PA1-921 detects recombinant rat beta-epithelial sodium channel (beta-ENaC). PA1-921 has been successfully used in immunoprecipitation procedures. By immunoprecipitation this antibody specifically binds to the unglycosylated, ~75 kDa recombinant rat beta-ENaC protein. This product fails to detect beta-ENaC protein in Western blot procedures. PA1-921 immunizing peptide corresponds to amino acid residues 619-640 from human beta-ENaC. This sequence is 90% and 81% conserved in the rabbit, rat and mouse beta-ENaC, respectively. PA1-921 immunizing peptide (Cat. # PEP-089) is available for use in neutralization and control experiments. |
| General 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). |
| References: |
| Am. J. Physiol. 273 (Gastrointest. Liver Physiol., 36): G571-G585, 1997. |
| Biochem. Biophys. Res. Comm., 245:589-593, 1998. |