Tumor necrosis factor receptor superfamily member 21

Definition:

Promotes apoptosis, possibly via a pathway that involves the activation of NF-kappa-B. Can also promote apoptosis mediated by BAX and by the release of cytochrome c from the mitochondria into 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 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; this triggers caspase activation and degeneration of both neuronal cell bodies (via caspase-3) and axons (via caspase-6). Negatively regulates oligodendrocyte survival, maturation and myelination. Plays a role in signaling cascades triggered by stimulation of T-cell receptors, in the adaptive immune response and in the regulation of T-cell differentiation and proliferation. Negatively regulates T-cell responses and the release of cytokines such as IL4, IL5, IL10, IL13 and IFNG by Th2 cells. Negatively regulates the production of IgG, IgM and IgM in response to antigens. May inhibit the activation of JNK in response to T-cell stimulation.

References:

[1]. Sha Mi, et al. Death receptor 6 negatively regulates oligodendrocyte survival, maturation and myelination. Nat Med. 2011 Jul 3;17(7):816-21. [Content Brief]

[2]. G Pan, et al. Identification and functional characterization of DR6, a novel death domain-containing TNF receptor. FEBS Lett. 1998 Jul 24;431(3):351-6. [Content Brief]

[3]. Linlin Zeng, et al. Death receptor 6 induces apoptosis not through type I or type II pathways, but via a unique mitochondria-dependent pathway by interacting with Bax protein. J Biol Chem. 2012 Aug 17;287(34):29125-33. [Content Brief]

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