|Tested species reactivity||Rat|
|Host / Isotype||Rabbit / IgG|
|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|
|Purification||Antigen affinity chromatography|
|Storage buffer||PBS with 1mg/ml BSA|
|Contains||0.05% sodium azide|
|Storage Conditions||-20° C, Avoid Freeze/Thaw Cycles|
|Tested Applications||Dilution *|
|Immunoprecipitation (IP)||Assay dependent|
* Suggested working dilutions are given as a guide only. It is recommended that the user titrate the product for use in their own experiment using appropriate negative and positive controls.
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.
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 and quote;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.