Invitrogen™ FXR Polyclonal Antibody

FXR (farnesoid X receptor; NR1H4) belongs to nuclear receptor superfamily of ligand-activated transcription factors (NR1 subfamily) and acts as a receptor for bile acids such as chenodeoxycholic acid, lithocholic acid and deoxycholic acid. FXR plays an essential role in bile acid homeostasis through the regulation of genes involved in bile acid synthesis, conjugation and enterohepatic circulation. FXR also regulates lipid and glucose homeostasis and is involved innate immune response. The FXR-RXR heterodimer binds predominantly to farnesoid X receptor response elements (FXREs) containing two inverted repeats of the consensus sequence 5'-AGGTCA-3' in which the monomers are spaced by 1 nucleotide (IR-1) but also to tandem repeat DR1 sites with lower affinity, and can be activated by either FXR or RXR-specific ligands. In the liver FXR activates transcription of the corepressor NR0B2 thereby indirectly inhibiting CYP7A1 and CYP8B1 (involved in BA synthesis) implicating at least in part histone demethylase KDM1A resulting in epigenomic repression, and SLC10A1/NTCP (involved in hepatic uptake of conjugated BAs). FXR activates transcription of SLC27A5/BACS and BAAT (involved in BA conjugation), ABCB11/BSEP (involved in bile salt export) by directly recruiting histone methyltransferase CARM1, and ABCC2/MRP2 (involved in secretion of conjugated BAs) and ABCB4 (involved in secretion of phosphatidylcholine in the small intestine). (From Uniprot).