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. 2002 Apr 1;109(7):961–971. doi: 10.1172/JCI14505

Figure 9.

Figure 9

The RXR heterodimerization-incompetent FXR mutant Leu433Arg binds the C site and negatively regulates apoA-I promoter activity. (a) Gel retardation assays were performed on end-labeled IR-1 consensus (lanes 1–5) and wild-type C-site (lanes 6–9) oligonucleotides in the presence of unprogrammed reticulocyte lysate (lane 1) or in the presence of in vitro–transcribed/translated wild-type hFXR (lanes 2 and 6), mutant hFXR Leu433Arg (lanes 4 and 8), or both mRXR and wild-type (lanes 3 and 7) or mutant Leu433Arg (lanes 5 and 9) hFXR proteins. (b and c) HepG2 cells were transfected with a IR-1–driven (b) or apoA-I promoter–driven (c) reporter vectors (1 μg) in the presence of either the pcDNA3 wild-type or mutated FXR- and RXR-containing expression vectors (300 ng) as indicated. Cells were subsequently treated with CDCA (75 μM) or vehicle for 36 hours. Values are expressed as percentage of control set at 100% normalized to internal control β-galactosidase activity as described in Methods. FXRE, FXR response element.