Nuclear pregnane x receptor and constitutive androstane receptor regulate overlapping but distinct sets of genes involved in xenobiotic detoxification.
By J. M. Maglich, C. Stoltz, B. Goodwin, D. Hawkins-Brown, John T. Moore, S. Kliewer. Molecular Pharmacology, 2002
686 citations recorded by the source corpus.
Subfields: Endocrinology, Diabetes and Metabolism, Genetics, Pharmacology
View Paper: https://www.semanticscholar.org/paper/4e525c18db6bd66f0cc58930ce49cb65db8a934b
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In Genetics
In Pharmacology
Citations in the corpus
- Induction of phase I, II and III drug metabolism/transport by xenobiotics (2005, background): “…studies indicated that activation of CAR is a multistep process, the initial step is nuclear translocation, which can be independent of ligand binding, the final step is CaMK-dependent activation of this receptor (Bae et aL, 2004; Maglich et aL, 2002; Paquet et al., 2000; Wang and LeCluyse, 2003).”
- The Human Obesity Gene Map: The 2005 Update (2006, background): “3 NR1I3 Nuclear receptor subfamily 1, group I, member 3 Accelerated adipose loss on calorierestricted diet (485)”
- Xenobiotic, Bile Acid, and Cholesterol Transporters: Function and Regulation (2010, neutral): “21 and 22) (Maglich et al., 2002; Staudinger et al., 2003; Teng et al., 2003; Maher et al., 2005a; Cheng and Klaassen, 2006).”
- Cytochrome P450 enzymes in drug metabolism: regulation of gene expression, enzyme activities, and impact of genetic variation. (2013, background): “All three expressed CYP2C enzymes are inducible by ligands of the PXR/CAR, glucocorticoid (GR) and vitamin D (VDR) nuclear receptor pathways through different response elements in their 5′-flanking regions (Chen & Goldstein, 2009; Jover et al., 2009; Helsby & Burns, 2012).”
- Recent advances in 2D and 3D in vitro systems using primary hepatocytes, alternative hepatocyte sources and non-parenchymal liver cells and their use in investigating mechanisms of hepatotoxicity, cell signaling and ADME (2013, positive): “FXR appears to act as a cell protecting biosensor for intestinal and hepatic cells against bile acid overload by (1) increasing the expression of transport proteins that support the elimination of bile acids from the cell (BSEP, MRP2) and bile acid detoxification (Maglich et al. 2002; Synold et al. ”