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.
Biological Process: axon guidance; caspase activation; circadian regulation of gene expression; glucose homeostasis; immune response; inflammatory response; intracellular protein transport; membrane protein intracellular domain proteolysis; negative regulation of apoptosis; negative regulation of axonogenesis; negative regulation of caspase activity; negative regulation of mitochondrial depolarization; negative regulation of neuron apoptosis; nerve growth factor receptor signaling pathway; positive regulation of apoptosis; positive regulation of axonogenesis; positive regulation of MAPKKK cascade; positive regulation of myelination; positive regulation of protein kinase B signaling cascade; positive regulation of Rho protein signal transduction; positive regulation of synaptic transmission, cholinergic; positive regulation of synaptic transmission, glutamatergic; regulation of apoptosis; regulation of caspase activity; regulation of cell proliferation; response to lipopolysaccharide; response to wounding; sensory perception of pain; tumor necrosis factor-mediated signaling pathway
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.