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. 2009 May 29;284(22):15071–15083. doi: 10.1074/jbc.M109.006742

FIGURE 1.

FIGURE 1.

Identification of LXRE in the LGK gene promoter. A, Alexander cells were cotransfected with 100 ng of expression vectors for LXRα and/or RXRα and luciferase reporters under the control of rat LGK promoters (pRGKL-1448). After 24 h, the cells were treated with T1317 (1 μm) and/or 9-CR (1 μm) for 24 h. White bar, negative control; gray bar, T1317; dark gray bar, 9-CR; black bar, T1317- and 9-CR-treated group. B, 5′ serial deletion constructs of the LGK gene promoter reporter were transfected into Alexander cells. The positions of mutations are shown in Fig. 2C. D, luciferase reporter constructs containing mutants in the LGK gene promoter were transfected into Alexander cells. The cells were cotransfected with the expression vectors for LXRα and RXRα in the presence or absence of T1317 and 9-CR. White bar, no transfection of LXRα and RXRα and no treatment with 9-CR and T1317; black bar, transfection of LXRα and RXRα and treatment with T1317 and 9-CR (B and D). Normalized luciferase activities are shown as the mean ± S.D. of three independent experiments performed in triplicate and are expressed as -fold increases relative to the basal activity.