功能 |
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.
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總結 |
Apoptosis is induced by certain cytokines including TNF and Fas ligand of the TNF family thro μgh their death domain containing receptors, TNF-R1 and Fas. Several novel death receptor including DR3, DR4, and DR5 were recently identified. A new death domain containing receptor in the TNFR family was cloned recently and termed DR6 for death receptor 6. Like TNF-R1, DR6 interacts with death domain containing adapter molecule TRADD. Overexpression of DR6 induces apoptosis and activates NF-kB and JNK. DR6 is widely expressed in human tissues and cell lines.
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