The farnesoid X receptor (FXR) is a nuclear hormone receptor and can function as a ligand inducible transcription factor capable of acting as a co-repressor and/or co-activator for gene expression. Nuclear receptors contain a series of conserved domains or regions. These domains/regions include a variable NH2-domain (A/B region), a conserved DNA-binding domain (DBD or region C), a linker region (region D), a ligand binding domain (LBD or region E), and in some receptors a variable COOHterminal (region F). The FXR nuclear receptor forms a heterodimer with RXR (retinoid X receptor) that recognizes an inverted repeat of the AGGTCA sequence with no spacing and 1 base-spacing. The FXR-RXR heterodimer can recognize additional direct repeats with different binding affinities. When bound the FXR-RXR heterodimer can function as a transcription activator or inhibitor. When a ligand interacts with the FXR ligand binding domain the receptor undergoes conformational changes. These conformational changes lead to a decrease in the affinity of transcription co-repressors and the interaction with transcription co-activators. These co-activators and co-repressors regulate gene transcription by interacting with the transcriptional pre-initiation complex and histone acetyl transferases. The interaction of nuclear receptors and FXR with these co-activators and corepressors may be ligand specific. FXR is activated by bile acids and regulates the expression of genes involved in bile acid synthesis, cholesterol metabolism, and plasma triglyceride concentrations. The primary agonist for FXR is chenodeoxycholic acid (CDCA). Additional bile acids function as partial agonists for FXR including: deoxycholic acid (DCA), cholic acid (CA), and ursodeoxycholic acid (UDCA). FXR is expressed in the liver, intestine, kidney and adrenal cortex. FXR reduces bile acid concentration in heptocytes by repressing genes involved in the bile acid biosynthetic pathway (CYP7A1, CYP8B1, and CYP27A1), and regulates triglyceride and lipoprotein metabolism by increasing the expression of apolipoprotein and lipoprotein enzymes (PLTP and APOCII).