Tumor necrosis factor receptor superfamily member 21 (TNFRSF21)

Promotes apoptosis, possibly by means of a pathway that involves the activation of NF-kappa-B. Can also promote apoptosis mediated by BAX and from the release of cytochrome c from the mitochondria to the cytoplasm.

Plays a role in neuronal apoptosis, including apoptosis in response to amyloid peptides derived from APP, and is required for both normal cell body death and axonal pruning. Trophic-factor deprivation activates 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).