Render Target: STATIC
Render Timestamp: 2024-12-20T10:56:39.622Z
Commit: f2d32940205a64f990b886d724ccee2c9935daff
XML generation date: 2024-09-30 01:57:53.103
Product last modified at: 2024-12-17T18:58:00.214Z
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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77
R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

Mineralocorticoid Receptor (E9W1M) Rabbit mAb #58883

Filter:
  • WB
  • IP

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 120
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:50

    Storage

    Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    Mineralocorticoid Receptor (E9W1M) Rabbit mAb recognizes endogenous levels of total mineralocorticoid receptor protein.

    Species Reactivity:

    Human

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with recombinant protein specific to the amino terminus of human mineralocorticoid receptor protein.

    Background

    Mineralocorticoid receptor (MR) is a steroid hormone receptor with structural and functional similarities to glucocorticoid receptor (GR). MR binds with high affinity to aldosterone and other mineralocorticoids as well as glucocorticoids (1-3). Upon ligand binding, MR undergoes conformational changes and enters the nucleus to bind to target mineralocorticoid response elements (MREs) (3-5). MR is also able to heterodimerize with GR and bind to hormone response elements on DNA in cells that express both receptors (6-8). Unlike the anti-inflammatory activity of GR, aldosterone and MR can promote cardiovascular inflammation (9,10). Since MR can utilize both aldosterone and glucocorticoids as ligands, selectivity of ligands is facilitated by tissue-specific expression of 11 beta-hydroxysteroid dehydrogenase (11 beta-OHSD). This enzyme converts cortisol to cortisone, a derivative with very little affinity to MR, thus providing a means for tissue-specific MR regulation (11,12). Deficiency of 11 beta-OHSD has shown to cause an excess of MR signaling resulting in hypertension (12,13). Antimineralocorticoid spirolactones have been used as synthetic steroids to induce a transcriptionally inactivated conformational change in MR to treat hypertension and sodium retention (14,15).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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