Molecular basis for feedback regulation of bile acid synthesis by nuclear receptors.

By T. T. Lu, M. Makishima, J. Repa, K. Schoonjans, T. A. Kerr, Johan Auwerx, D. Mangelsdorf. Molecules and Cells, 2000

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Definition of a novel growth factor-dependent signal cascade for the suppression of bile acid biosynthesis. (2003, background): “…the molecular mechanisms by which bile acids suppress CYP7A1 expression, and it is now apparent that multiple, redundant pathways exist (Stravitz et al. 1995; Antes et al. 2000; Goodwin et al. 2000; Lu et al. 2000; Miyake et al. 2000; De Fabiani et al. 2001; Kerr et al. 2002; Wang et al. 2002).”
Effects of infection and inflammation on lipid and lipoprotein metabolism: mechanisms and consequences to the host. (2004, neutral): “In contrast, increases in FXR/RXR activation reduce CYP7A1 activity by increasing small heterodimer partner (SHP), which in turn blocks the ability of the transcription factor liver receptor homolog-1 (LRH-1), to stimulate CYP7A1 expression (220).”
Nuclear receptors — a perspective from Drosophila (2005, background): “These cross-regulatory interactions among fly orphan receptors provide an interesting parallel to studies of regulatory specificity that are conferred by vertebrate nuclear-receptor interaction”
Farnesoid X receptor is essential for normal glucose homeostasis. (2006, methodology): “Feeding a 1% CA diet for 5 days increased SHP expression in WT mice and strongly decreased CYP7A1 expression, as expected (4, 11, 24).”