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Patricia C. Chui, Hong-Ping Guan, Michael Lehrke, Mitchell A. Lazar
Published in Volume 115, Issue 8
J Clin Invest. 2005; 115(8):2244–2256 doi:10.1172/JCI24130
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Figure 3

The proximal PPARγ binding site in the OLR1 promoter is the predominant PPRE. (A) Identification of putative PPARγ binding sites (underlined) in the OLR1 promoter. Letters A–D correspond to arrowheads in Figure 2A. (B) DNA mobility shift assay showing the binding of PPARγ/RXRα to wild-type and mutant oligonucleotide probes corresponding to the putative PPARγ binding sites underlined in A. Control lane reactions did not contain PPARγ/RXRα. Mutant oligonucleotides contain point mutations in the putative PPARγ binding site; for specific mutations, see Methods. (C) Luciferase activity of OLR1 reporter constructs containing mutations in the PPARγ binding sites. Site-specific mutations were made in the longest OLR1 reporter construct (–1,738; Figure 2A). Data represent the fold induction of luciferase activity over the basal activity of the empty pGL2 vector and are expressed as mean ± SEM (n = 3 per condition). *P < 0.01 compared with transfected cells treated with vehicle.