Ligand-activated transcription factor. Key regulator of lipid metabolism. Activated by the endogenous ligand 1-palmitoyl- 2-oleoyl-sn-glycerol-3-phosphocholine (16:0/18:1-GPC). Activated by oleylethanolamide, a naturally occurring lipid that regulates satiety. Receptor for peroxisome proliferators such as hypolipidemic drugs and fatty acids. Regulates the peroxisomal beta-oxidation pathway of fatty acids. Functions as transcription activator for the ACOX1 and P450 genes. Transactivation activity requires heterodimerization with RXRA and is antagonized by NR2C2. Belongs to the nuclear hormone receptor family. NR1 subfamily. Note: This description may include information from UniProtKB.
Molecular Function: DNA binding; drug binding; ligand-dependent nuclear receptor activity; lipid binding; NFAT protein binding; phosphatase binding; protein binding; protein complex binding; protein domain specific binding; sequence-specific DNA binding; steroid hormone receptor activity; transcription factor activity; ubiquitin conjugating enzyme binding; zinc ion binding
Biological Process: behavioral response to nicotine; cellular lipid metabolic process; circadian regulation of gene expression; epidermis development; fatty acid metabolic process; fatty acid transport; heart development; intracellular receptor-mediated signaling pathway; lipid metabolic process; lipoprotein metabolic process; negative regulation of appetite; negative regulation of blood pressure; negative regulation of glycolysis; negative regulation of inflammatory response; negative regulation of protein binding; negative regulation of transcription from RNA polymerase II promoter; positive regulation of fatty acid beta-oxidation; positive regulation of fatty acid oxidation; positive regulation of gluconeogenesis; positive regulation of transcription from RNA polymerase II promoter; positive regulation of transcription, DNA-dependent; regulation of circadian rhythm; response to hypoxia; response to insulin stimulus; steroid hormone mediated signaling; transcription initiation from RNA polymerase II promoter; wound healing
LTP: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.