Anti-LXR alpha (NR1H3)

0.5mg/ml if reconstituted with 0.2ml sterile DI water. Liver X receptor alpha, also called NR1H3, is a tissue-specific cofactor that permits RXRA to function as a potent 9cRA receptor with a distinct target gene specificity. It specifically interacts with RXRA in vivo to form a functional heterodimer in which RXRA is the ligand-binding subunit. Additionally, Liver X receptor activity is critical for physiologic lipid metabolism and transport. They are endogenous inhibitors of atherogenesis and are targets for therapeutic intervention in cardiovascular disease. Furthermore, they and their ligands are negative regulators of macrophage inflammatory gene expression. Liver X receptors act as a transcriptional switch that integrates hepatic glucose metabolism and fatty acid synthesis. The LXR-IDOL-LDLR axis defines a complementary pathway to sterol response element-binding proteins for sterol regulation of cholesterol uptake. Protein function: Nuclear receptor. Interaction with RXR shifts RXR from its role as a silent DNA-binding partner to an active ligand- binding subunit in mediating retinoid responses through target genes defined by LXRES. LXRES are DR4-type response elements characterized by direct repeats of two similar hexanuclotide half- sites spaced by four nucleotides. Plays an important role in the regulation of cholesterol homeostasis, regulating cholesterol uptake through MYLIP-dependent ubiquitination of LDLR, VLDLR and LRP8. Interplays functionally with RORA for the regulation of genes involved in liver metabolism. Exhibits a ligand-dependent transcriptional activation activity (PubMed:25661920). [The UniProt Consortium]