FIGURE 6.

SHP inhibits LXRα and PPARγ-mediated LGK promoter activity. Alexander cells were cotransfected with expression vectors for LXRα (100 ng) and RXRα (100 ng) (A) or PPARγ (100 ng) and RXRα (100 ng) (B) with SHP expression vector and LGK promoter-luciferase reporter (pRGKL-1448). Cells were treated with their respective ligands. Normalized luciferase activities are shown as mean ± S.D. of three independent experiments in triplicate and are expressed as -fold increase relative to the basal activity. The expression of HA-SHP protein was validated by immunoblotting (A and B). Rat primary cultured hepatocytes were transduced by adenoviral expression of SHP. After 3 h, T1317 (1 μm)/9-CR (1 μm) (C) or rosiglitazone (1 μm)/9-CR (1 μm) (D) were treated for 24 h. The transcription levels of LGK and expression of SHP were quantitated by real-time PCR (C and D).