KLH conjugated synthetic peptide derived from human FXR/Bile Acid Receptor NR1H4.
Conjugation:
Unconjugated
Alternative Names:
Bile acid receptor, Farnesoid X-activated receptor, Farnesol receptor HRR-1, Nuclear receptor subfamily 1 group H member 4, Retinoid X receptor-interacting protein 14, RXR-interacting protein 14, NR1H4, BAR, FXR, HRR1, RIP14
The farnesoid X receptor (FXR/NR1H4) is a member of the nuclear hormone receptor superfamily and is a master regulator of bile acid synthesis. FXR/NR1H4 heterodimerizes with RXR-alpha upon activation by bile acids, which begins a regulatory cascade involving SHP and LRH-1 to control lipid homeostasis. FXR/NR1H4 has also been shown to be a critical regulator of glucose homeostasis. In addition to directly regulating genes, FXR/NR1H4 also plays a post transcriptional role in bile acid metabolism by transcribing the RNA-binding protein ZFP36L1, which in turn downregulates the key enzyme Cyp7a1. Mutations in human FXR/NR1H4 have been shown to cause cholestasis and liver disease in neonatal patients. FXR/NR1H4 can also control Lgr5+ intestinal stem cell proliferation and its upregulation has been shown to inhibit colorectal cancer progression. Agonists against FXR/NR1H4 are being evaluated for various liver diseases and diabetes.
The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen and the purity is > 95% (by SDS-PAGE).
Form:
Rabbit IgG, 1mg/ml in PBS with 0.02% sodium azide, 50% glycerol, pH7.2
