There is evidence that a group of closely related nuclear receptors, called peroxisome proliferator-activated receptors (PPARs), may be involved in chronic diseases such as diabetes, obesity, artherosclerosis and cancer. The PPARs were first cloned as the nuclear receptors that mediate the effects of synthetic compounds called peroxisome proliferators on gene transcription. It soon became clear that eicosanoids and fatty acids can also regulate gene transcription through PPARs. They bind a specific element in the promoter region of target genes only as a heterodimer with the receptor for 9- cis retinoic acid, RXR (retinoid X receptor). Binding of the ligand of either receptor can activate the complex, but binding of both ligands simultaneously is more potent (1). Three PPAR isotypes have been identified: α, β (also called NUC1) and γ. PPARβ is found in many tissues but the highest expression is in the gut, kidney and heart (2). PPARβ or PPARδ have received little attention, probably because of the lack of a connection with important clinical manifestations. However, recently PPARβ has been linked to colon cancer (3) and as an inducer of COX-2 expression in carcinogenesis, among other functions. PPAR regulates the expression of acyl-CoA synthetase 2 in the brain, linking PPARβ to basic lipid metabolism (4). Moreover, it probably participates in embryo implantation and decidualization (5).
Synonym : FAAR; MGC3931; NR1C2; NUC1; NUCI; NUCII;PPARB and Homo sapiens peroxisome proliferator-activated receptor delta (PPARD).
Recombinant GST-PPARδ-LBD is isolated from an E. coli strain that carries the coding sequence of the human PPARδ under the control of a T7 promoter. GST-PPARδ-LBD can be applied in protein-protein interaction assays. Purified protein is greater than 95% homogeneous based on SDS-PAGE analysis. 1 unit equals 1 nanogram of purified protein. variable in different lots 1x dilution buffer A: 20 mM Tris-Cl (pH 8.0), 20% Glycerol, 100 mM KCl, 1 mM DTT and 0.2 mM EDTA
References: 1. Desvergene et al., (1999) Endocr. Rev. 20, 649-688 2. Kersten (2000) Nature 405, 421-424 3. He et al., (1999) Cell 99, 335-345 4. Basu-Modak et al., (1999) J. Biol. Chem. 274, 35881-35888 5. Lim et al., (1999) genes Dev. 13, 1561-1574
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