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.
Protein type: Nuclear receptor; DNA binding protein
Cellular Component: nucleoplasm; nucleus
Molecular Function: protein domain specific binding; ligand-dependent nuclear receptor activity; NFAT protein binding; zinc ion binding; drug binding; phosphatase binding; protein binding; DNA binding; ubiquitin conjugating enzyme binding; sequence-specific DNA binding; protein complex binding; steroid hormone receptor activity; transcription factor activity; lipid binding
Biological Process: transcription initiation from RNA polymerase II promoter; epidermis development; intracellular receptor-mediated signaling pathway; wound healing; positive regulation of transcription, DNA-dependent; heart development; behavioral response to nicotine; lipoprotein metabolic process; negative regulation of transcription from RNA polymerase II promoter; cellular lipid metabolic process; fatty acid metabolic process; negative regulation of appetite; response to insulin stimulus; positive regulation of fatty acid beta-oxidation; positive regulation of fatty acid oxidation; response to hypoxia; positive regulation of transcription from RNA polymerase II promoter; gene expression; negative regulation of blood pressure; lipid metabolic process; negative regulation of protein binding; negative regulation of glycolysis; fatty acid transport
SS: 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.