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Results: 9

1.
FIGURE 9.

FIGURE 9. From: Regulation of Cholesterologenesis by the Oxysterol Receptor, LXR?.

Model illustrating the roles of LXR and SREBP in regulation of cholesterol biosynthesis.

Yongjun Wang, et al. J Biol Chem. 2008 September 26;283(39):26332-26339.
2.
FIGURE 4.

FIGURE 4. From: Regulation of Cholesterologenesis by the Oxysterol Receptor, LXR?.

Regulation of cholesterol biosynthesis by LXRα. a, LXRα depletion increases cholesterol content in HepG2 cells. b, LXRα depletion results in an increase in cholesterol biosynthesis in HepG2 cells. *, p < 0.05 versus control as determined by Student's t test.

Yongjun Wang, et al. J Biol Chem. 2008 September 26;283(39):26332-26339.
3.
FIGURE 1.

FIGURE 1. From: Regulation of Cholesterologenesis by the Oxysterol Receptor, LXR?.

Identification of LXRα occupancy sites in the regulatory regions of cholesterol biosynthetic enzyme genes. a, schematic outlining the cholesterol biosynthetic process identifying the position of HMGCR, FDFT1, and CYP51A1 in the process. b, position of LXRα occupancy within the CYP51A1 and FDFT1 genes as determined by ChIP-on-chip.

Yongjun Wang, et al. J Biol Chem. 2008 September 26;283(39):26332-26339.
4.
FIGURE 3.

FIGURE 3. From: Regulation of Cholesterologenesis by the Oxysterol Receptor, LXR?.

Regulation of HMGCR expression and activity by LXRα. a, LXRα depletion causes an increase in HMGCR protein expression in HepG2 cells. b, LXRα depletion results in an increase in HMGCR activity in HepG2 cells. *, p < 0.05 versus control as determined by Student's t test.

Yongjun Wang, et al. J Biol Chem. 2008 September 26;283(39):26332-26339.
5.
FIGURE 5.

FIGURE 5. From: Regulation of Cholesterologenesis by the Oxysterol Receptor, LXR?.

Identification of LXR-binding sites (LXREs) within the CYP51A1 and FDFT1 genes. a, location and sequence of the putative LXRE identified in the CYP51A1 promoter and the first intron of FDFT1 compared with the LXREs of the NR1H3 and ABCA1 genes. b, electrophoretic mobility shift assay illustrating the ability of LXRα/RXRα to bind to the CYP51A1 and FDFT1 LXREs. A competition experiment was performed with the either the CYP51A1 or FDFT1 LXRE as the labeled probe, and the binding was competed with either cold CYP51A1 or FDFT1 oligonucleotide (5×, 25×, and 100× molar excess) or ABCA1 LXRE oligonucleotide (5×, 25×, and 100× molar excess).

Yongjun Wang, et al. J Biol Chem. 2008 September 26;283(39):26332-26339.
6.
FIGURE 2.

FIGURE 2. From: Regulation of Cholesterologenesis by the Oxysterol Receptor, LXR?.

Regulation of expression of CYP51A1 and FDFT1 expression by LXRα. a, specific LXRα siRNA treatment depletes both LXRα mRNA and LXRα protein expression in HepG2 cells. b, LXRα depletion results in increased expression of CYP51A1 and FDFT1 mRNA in HepG2 cells. C, LXRα depletion results in increased expression of CYP51A1 and FDFT1 protein. A Western blot showing LXRα expression levels from an example experiment is illustrated. The lanes are from the same gel, and we treated and analyzed it in an identical manner. *, p < 0.05 versus control as determined by Student's t test.

Yongjun Wang, et al. J Biol Chem. 2008 September 26;283(39):26332-26339.
7.
FIGURE 6.

FIGURE 6. From: Regulation of Cholesterologenesis by the Oxysterol Receptor, LXR?.

The nLXREs from the CYP51A1 and FDFT1 genes confer oxysterol-dependent repression to a reporter gene in HepG2 cells. a, the nLXREs from both the CYP51A1 and FDFT1 genes mediate repression of basal transcription when cloned upstream of a minimal promoter luciferase reporter, whereas the positive LXRE mediates moderate stimulation of transcription in transfected HepG2 cells. b, effects of various LXR ligands on a luciferase reporter harboring three copies of the NR1H3 LXRE upstream of a minimal promoter when transfected in to HepG2 cells. c, effects of various LXR ligands on a luciferase reporter harboring three copies of the CYP51A1 LXRE upstream of a minimal promoter when transfected in to HepG2 cells. d, effects of various LXR ligands on a luciferase reporter harboring three copies of the FDFT1 LXRE upstream of a minimal promoter when transfected in to HepG2 cells. All of the experiments within this figure utilized lipid depleted media as described under “Experimental Procedures.” Synthetic LXR ligands T1317 and GW3965 were tested at 1 μm, and the oxysterols were tested at 10 μm. Me2SO concentrations in all wells were held constant at 0.1%. *, p < 0.05 versus control as determined by Student's t test.

Yongjun Wang, et al. J Biol Chem. 2008 September 26;283(39):26332-26339.
8.
FIGURE 7.

FIGURE 7. From: Regulation of Cholesterologenesis by the Oxysterol Receptor, LXR?.

The nLXREs from the CYP51A1 and FDFT1 genes confer oxysterol-dependent repression to a reporter gene in HEK293 cells. a, HEK 293 cells were transfected with either LXRα or LXRβ and reporter genes containing either a positive LXRE or negative LXREs. The nLXREs from both the CYP51A1 and FDFT1 genes mediate repression of basal transcription when cloned upstream of a minimal promoter luciferase reporter, whereas the positive LXRE mediates stimulation of transcription. Control cells received empty expression vector instead of a vector directing the expression of LXR. b, effects of various LXR ligands on a luciferase reporter harboring three copies of the CYP51A1 LXRE upstream of a minimal promoter when transfected in HEK293 cells along with LXRα. c, effects of various LXR ligands on a luciferase reporter harboring three copies of the FDFT1 LXRE upstream of a minimal promoter when transfected in to HEK293 cells along with LXRα. All of the experiments within this figure utilized lipid depleted medium as described under “Experimental Procedures.” Synthetic LXR ligands T1317 and GW3965 were tested at 1 μm, and the oxysterols were tested at 10 μm. Me2SO concentrations in all wells were held constant at 0.1%. *, p < 0.05 versus control as determined by Student's t test.

Yongjun Wang, et al. J Biol Chem. 2008 September 26;283(39):26332-26339.
9.
FIGURE 8.

FIGURE 8. From: Regulation of Cholesterologenesis by the Oxysterol Receptor, LXR?.

Examination of the role of the nLXRE in the CYP51A1 promoter. a, LXRα depletion by siRNA treatment results in significant loss of the ability of 25-OHC to repress CYP51A1 expression in HepG2 cells. b, deletion analysis suggests that both the nLXRE and the SRE mediate a component of the ability of 25-OHC to repress transcription of a CYP51A1 promoter driven luciferase reporter in HepG2 cells. c, schematic illustrating the LXRE mutant that was created to eliminate LXR binding to the CYP51A1 promoter reporter construct. d, EMSA demonstrating that the mutant LXRE does not bind to LXRα. A competition experiment was performed with the wild type LXRE as the labeled probe, and the binding was competed with either cold wild type oligonucleotide (5×, 25×, and 100× molar excess) or mutant oligonucleotide (5×, 25×, and 100× molar excess). e, elimination of LXR binding results in reduced ability of 25-OHC to repress transcription of the CYP51A1 reporter. HepG2 cells were treated with 10 μm 25-OHC resulting in ∼72% repression of transcription of the wild type promoter but only ∼45% inhibition of transcription from the LXRE mutant CYP51A1 promoter. All of the experiments within this figure utilized lipid depleted medium as described under “Experimental Procedures.” Me2SO concentrations in all wells were held constant. *, p < 0.05 versus control as determined by Student's t test.

Yongjun Wang, et al. J Biol Chem. 2008 September 26;283(39):26332-26339.

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