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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Correlation of farnesoid X receptor coactivator recruitment and cholesterol 7alpha-hydroxylase gene repression by bile acids.

Cholesterol conversion to bile acids in the liver is regulated by the rate-limiting enzyme cholesterol 7alpha-hydroxylase (CYP7A1). CYP7A1 activity is regulated by feedback repression by bile acids at the transcriptional level. The farnesoid X receptor (FXR), a member of the nuclear hormone receptor superfamily, was recently demonstrated to function as the bile acid receptor and its high level of expression in the liver implicates it in the transcriptional regulation of CYP7A1. This study compares the potencies of various bile acids in their ability to mediate recruitment of the transcriptional coactivator protein, steroid receptor coactivator-1 ( SRC-1), to the FXR ligand binding domain with their ability to repress CYP7A1 expression in HepG2 cells. A mammalian two-hybrid assay was utilized to assess the ability of FXR to recruit SRC-1 in a ligand-dependent manner. Chenodeoxycholic acid (CDCA) was the most potent and efficacious compound in the SRC-1 recruitment assay (EC(50) = 11.7 microM) followed by deoxycholic acid (DCA; EC(50) = 19.0 microM). Ursodeoxycholic acid (UDCA) displayed minimal activity while cholic acid (CA) was inactive. In order to directly compare the potencies of the bile acids in the coactivator recruitment assay to their ability to repress CYP7A1 expression, a branched DNA assay was developed to rapidly measure CYP7A1 mRNA levels from HepG2 cells cultured in 96-well plates. The rank order and absolute potency was conserved (CDCA IC(50) = 8.7 microM, DCA IC(50) = 27.2 microM, UDCA and CA inactive) consistent with bile acid repression of CYP7A1 being mediated by FXR.[1]


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