Regular ArticleCorrelation of Farnesoid X Receptor Coactivator Recruitment and Cholesterol 7α-Hydroxylase Gene Repression by Bile Acids
References (25)
Nuclear orphan receptors control cholesterol catabolism
Cell
(1999)- et al.
Activation of the nuclear receptor LXR by oxysterols defines a new hormone response pathway
J Biol Chem
(1997) - et al.
Cholesterol and bile acid metabolism are impaired in mice lacking the nuclear oxysterol receptor LXRα
Cell
(1998) - et al.
The LXRs: A new class of oxysterol receptors
Curr Opin Gen Devel
(1998) - et al.
Endogenous bile acids are ligands for the nuclear receptor FXR/BAR
Mol Cell
(1999) - et al.
Hepatocyte nuclear factor 1 binds to and transactivates the human but not the rat CYP7A1 promoter
Biochem Biophys Res Commun
(1999) - et al.
Identification of a bile acid-responsive element in the human ilieal bile acid-binding protein gene
J Biol Chem
(1999) - et al.
Farnesoid X receptor responds to bile acids and represses cholesterol 7α-hydroxylase gene (CYP7A1) transcription
J Biol Chem
(2000) - et al.
Thyroid hormone response elements differentially modulate the interactions of thyroid hormone receptors with two receptor binding domains in the steroid receptor coactivator-1
J Biol Chem
(1998) - et al.
PPARγ activation induces the expression of the adipocyte fatty acid binding protein gene in human monocytes
Biochem Biophys Res Commun
(1999)
Steroid hormone receptors compete for factors that mediate their enhancer function
Cell
Regulation of cholesterol 7 α-hydroxylase gene expression in Hep-G2 cells
J Biol Chem
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Discovery of farnesoid X receptor and its role in bile acid metabolism
2022, Molecular and Cellular EndocrinologyDifferential modulation of FXR activity by chlorophacinone and ivermectin analogs
2016, Toxicology and Applied PharmacologyCitation Excerpt :It is known that bile acids regulate the transcription of CYP7A1 by feedback repression through FXR binding. Studies have shown that the ability of various bile acids to recruit transcriptional coactivator protein (e.g., SRC-1) to the ligand binding domain of FXR is consistent with their ability to repress Cyp7A1 mRNA levels (Bramlett et al., 2000). On the other hand, in vitro pharmacological studies on liver cells demonstrated that theonellasterol antagonized the expression of FXR target genes including ABCC4 for the multidrug resistance-associated protein 4 (MRP-4) by abolishing the release of nuclear corepressor NCoR from the promoter of genes (Renga et al., 2012), and the in vivo studies using mice with obstructive cholestasis showed that theonellasterol increased MRP-4 expression in the liver and protected mice from liver injury.
Cholesterol 7α-hydroxylase protects the liver from inflammation and fibrosis by maintaining cholesterol homeostasis
2016, Journal of Lipid ResearchCitation Excerpt :As shown in Fig. 4C, GW4064 significantly increased the interaction between FXR and p65 through the LBD of FXR, because the DBD and the hinge domain of FXR do not interact with p65. Ligand-activated FXR is known to recruit coactivators such as steroid receptor coactivator-1 (SRC-1) to activate target gene transcription (33). SRC-1 is also a coactivator of NF-κB (34).
Nuclear receptors as new perspective for the management of liver diseases
2011, GastroenterologyIdentification of farnesoid X receptor modulators by a fluorescence polarization-based interaction assay
2010, Analytical Biochemistry
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