May activate NF-kappa-B and promote apoptosis. May activate JNK and be involved in T-cell differentiation. Required for both normal cell body death and axonal pruning. Trophic-factor deprivation triggers the cleavage of surface APP by beta-secretase to release sAPP-beta which is further cleaved to release an N- terminal fragment of APP (N-APP). N-APP binds TNFRSF21 triggering caspase activation and degeneration of both neuronal cell bodies (via caspase-3) and axons (via caspase-6). Associates with TRADD. Interacts with N-APP. Highly expressed in heart, brain, placenta, pancreas, lymph node, thymus and prostate. Detected at lower levels in lung, skeletal muscle, kidney, testis, uterus, small intestine, colon, spleen, bone marrow and fetal liver. Very low levels were found in adult liver and peripheral blood leukocytes. Note: This description may include information from UniProtKB.
Protein type: Apoptosis; Receptor, cytokine; Membrane protein, integral
Cellular Component: axon; integral to plasma membrane; plasma membrane; intrinsic to plasma membrane
Molecular Function: protein binding
Biological Process: myelination; neuron apoptosis; adaptive immune response; negative regulation of T cell proliferation; negative regulation of myelination; apoptosis; regulation of oligodendrocyte differentiation; B cell apoptosis; cellular lipid metabolic process; negative regulation of B cell proliferation; T cell receptor signaling pathway; humoral immune response
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.