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. 2009 Dec;20(12):2546–2555. doi: 10.1681/ASN.2009070696

Figure 5.

Figure 5.

Transcriptional analysis and ligand screening are shown. (A) The 5′ region of human SLCO4C1. Potential cis-acting sequences are indicated. Met, first methionine. (B) Promoter activity of human SLCO4C1. Deletion constructs of the human SLCO4C1 promoter region were analyzed with 3-MC (5 μM). *P < 0.05 (n = 3 to 4 per group). (C) Enhancement of promoter activity of human SLCO4C1 with various compounds (concentration as indicated, μM). Quer, quercetin; t-BHQ, tert-butylhydroquinone; I3C, indole-3-carbinole; IS, indoxyl sulfate; Tauro, taurocholic acid; Prava, pravastatin; Fluva, fluvastatin. *P < 0.05 versus DMSO; #P < 0.05 versus H2O (n = 3 to 4 per group). (D) Effect of fluvastatin (10 μM) on human SLCO4C1 transcription. Deletion constructs and loss-of-function mutation construct in XRE motifs of human SLCO4C1 were examined. *P < 0.05 (n = 3 to 4 per group). (E) ChIP assay and Western blotting of 3-MC or fluvastatin-treated cells. (Top) After application of 3-MC (1 μM) or fluvastatin (10 μM), fixed cell extract was analyzed by mouse cyp1a1 XRE or human SLCO4C1 XRE PCR. (Bottom) Western blotting of nuclear and cytoplasmic fractions from HEK293T cells were stained with antibodies against AhR, Lamin B, or α-tubulin antibodies. Cy, cytosolic fraction; Nu, nuclear fraction. (F) Enhancement of human SLCO4C1 promoter activity with various statins (10 μM) using the minimal promoter region (−129). *P < 0.05; #P < 0.01 (n = 3 to 4 per group).