Recombinant Human Death Receptor 6/DR6/TNFRSF21/CD358 (C-Fc)

Source: Human Cells. MW :61.7kD. Recombinant Human Death Receptor 6 is produced by our Mammalian expression system and the target gene encoding Gln42-Leu350 is expressed with a Fc tag at the C-terminus. Tumor Necrosis Factor Receptor Superfamily Member 21 (TNFRSF21) is a type I transmembrane receptor that includes four extracellular cysteine-rich motifs and a cytoplasmic death domain. DR6 is highly expressed in heart, brain, placenta, pancreas, lymph node, thymus and prostate. DR6 may activate NF-kappa-B and JNK to promote apoptosis and T-cell differentiation. In addition, DR6 binds with N-APP, which is released by the deprivation of Trophic-factor. It triggers caspase activation and degeneration of both neuronal cell bodies (via caspase-3) and axons (via caspase-6). DR6 is also expressed on the tumor cell lines and can be induced by TNF-a. Protein function: 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. [The UniProt Consortium]