Low affinity receptor which can bind to NGF, BDNF, NT-3, and NT-4. Can mediate cell survival as well as cell death of neural cells. Homodimer; disulfide-linked. Interacts with p75NTR- associated cell death executor. Interacts with TRAF2, TRAF4, TRAF6, PTPN13 and RANBP9. Interacts through TRAF6 with SQSTM1 which bridges NGFR to NTRK1. Interacts with BEX1 and NGFRAP1/BEX3. Interacts with KIDINS220 and NTRK1. Can form a ternary complex with NTRK1 and KIDINS220 and this complex is affected by the expression levels of KIDINS220. An increase in KIDINS220 expression leads to a decreased association of NGFR and NTRK1. Interacts with NTRK2; may regulate the ligand specificity of the NTRK2 receptor. Interacts with LINGO1. Note: This description may include information from UniProtKB.
Protein type: Membrane protein, integral; Receptor, misc.
Cellular Component: nucleoplasm; cell surface; integral to plasma membrane; extracellular region; plasma membrane; cytosol; endosome
Molecular Function: protein binding; signal transducer activity; transmembrane receptor activity; ubiquitin protein ligase binding; death receptor activity; nerve growth factor binding; receptor activity; Rab GTPase binding
Biological Process: axon guidance; detection of temperature stimulus; hair follicle morphogenesis; membrane protein intracellular domain proteolysis; central nervous system development; nerve growth factor receptor signaling pathway; positive regulation of apoptosis; negative regulation of fibroblast growth factor receptor signaling pathway; positive regulation of odontogenesis of dentine-containing teeth; regulation of caspase activity; regulation of axonogenesis; glucose homeostasis; negative regulation of hair follicle development; negative regulation of cell cycle; intracellular protein transport; positive regulation of fibroblast proliferation; nerve development; positive regulation of axonogenesis; negative regulation of axonogenesis; circadian regulation of gene expression; negative regulation of apoptosis
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.