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Anti -RXR (anti-RXR-LBD) antibody

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Description:

α-RXR antibody is an affinity-purified rabbit polyclonal antibody raised against the recombinant ligand-binding domain of the RXR protein.

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SKUPrice
PA114-01 $313.50
 

 Retinoid X receptor (RXR) serves as a promiscuous heterodimerization partner for many nuclear receptors through the identity box, a 40-amino acid subregion within the ligand binding domain (LBD). RXR partners include thyroid hormone receptors (TRs), retinoic acid receptors (RARs), peroxisome proliferator-activated receptor, several constitutive active orphan nuclear receptors (e.g. nuclear growth factor I-B), oxysterol receptors, and constitutive androstane receptors. RXRs also form homodimers to mediate the effects of 9-cis-retinoic acid (9-cRA). Depending on these protein-protein interactions, RXR-containing complexes have distinct ligand-dependent and constitutive functions (1, 2). The LBD is functionally complex and mediates ligand binding, receptor homo- and heterodimerization, repression of transcription in the absence of ligand, and ligand-dependent activation of transcription (3). Hormone binding to the structurally conserved LBD of the RXR triggers a conformational change that principally affects the conserved C-terminal transactivation helix H12 involved in transcriptional activation (4). Coactivators directly recruited by liganded receptors include members of the steroid receptor coactivator/p160 family such as SRC-1, transcriptional intermediary factor 2/glucocorticoid receptor interacting protein 1, and RAC3/activator of thyroid and retinoic acid receptors/amplified in breast cancer 1 (5).

Each vial contains 100 mg IgG in 0.1 ml of PBS.

Specificity
α-RXR reacts with the RXR protein in HeLa nuclear extract by Western Blotting. Recommended dilution range for Western blot analysis: 1:2000-1:5000. Recommended starting dilution: 1:2000.

Storage
Aliquot and store at –20°C.
 
References:
1. Mangelsdorf et al., (1995) Cell 83, 841-850
2. Mangelsdorf et al., (1995) Cell 83, 835-839
3. Nakashima et al., (1999) Science 284, 479-482
4. Egea et al., (2001) J. Mol. Biol. 307, 557-576
5. Leo et al., (2000) Gene 245, 1-11



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