an orphan nuclear receptor and immediate-early gene that regulates cellular proliferation, apoptosis, inflammation, and glucose metabolism. Induced by exercise in muscle and is a functional regulator of glucose metabolism in skeletal muscle. Its level decreases in the muscle of obese insulin-resistant men. Acts concomitantly with NURR1 in regulating the expression of delayed-early genes during liver regeneration. Binds the NGFI-B response element (NBRE) 5'-AAAAGGTCA-3'. May inhibit NF-kappa-B transactivation of IL2. A mediator of TCR-directed thymocyte apoptosis. TCR-signaling induces a FAIM/Akt/Nur77 signaling pathway that is critical for modulating apoptosis in developing thymocytes. A physiological substrate of the MEK-ERK-RSK cascade that modulates nuclear export and intracellular translocation during T cell death. Binds DNA as a monomer. Interacts with GADD45GIP1. Overexpression of Nur77 induces the expression of both p300 and HDAC1. Acetylation by p300 and HDAC1 may regulate the rapid turnover of Nur77 protein. Note: This description may include information from UniProtKB.
Protein type: Nuclear receptor; Apoptosis; DNA-binding
Molecular Function: protein binding; ligand-dependent nuclear receptor activity; DNA binding; zinc ion binding; sequence-specific DNA binding; protein heterodimerization activity; steroid hormone receptor activity
Biological Process: fat cell differentiation; epidermal growth factor receptor signaling pathway; transcription initiation from RNA polymerase II promoter; intracellular receptor-mediated signaling pathway; phosphoinositide-mediated signaling; fibroblast growth factor receptor signaling pathway; nerve growth factor receptor signaling pathway; signal transduction; negative regulation of cell cycle; cell migration during sprouting angiogenesis; innate immune response; steroid hormone mediated signaling; gene expression; positive regulation of transcription from RNA polymerase II promoter; positive regulation of endothelial cell proliferation
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.