Death receptor 5
Appearance
Template:PBB Tumor necrosis factor receptor superfamily, member 10b, official symbol TNFRSF10B, is a human gene. Also known as: DR5, CD262, KILLER, TRICK2, TRICKB, ZTNFR9, TRAILR2, TRICK2A, TRICK2B, TRAIL-R2, KILLER/DR5
Interactions
TNFRSF10B has been shown to interact with FADD,[1][2] TRAIL,[3][4][5] Caspase 10[1][6] and Caspase 8.[1][6]
See also
References
- ^ a b c Gajate, Consuelo (2005). "Cytoskeleton-mediated death receptor and ligand concentration in lipid rafts forms apoptosis-promoting clusters in cancer chemotherapy". J. Biol. Chem. 280 (12). United States: 11641–7. doi:10.1074/jbc.M411781200. ISSN 0021-9258. PMID 15659383.
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ignored (help)CS1 maint: unflagged free DOI (link) - ^ Chaudhary, P M (1997). "Death receptor 5, a new member of the TNFR family, and DR4 induce FADD-dependent apoptosis and activate the NF-kappaB pathway". Immunity. 7 (6). UNITED STATES: 821–30. doi:10.1016/S1074-7613(00)80400-8. ISSN 1074-7613. PMID 9430227.
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ignored (help) - ^ Kaptein, A (2000). "Studies on the interaction between TWEAK and the death receptor WSL-1/TRAMP (DR3)". FEBS Lett. 485 (2–3). NETHERLANDS: 135–41. doi:10.1016/S0014-5793(00)02219-5. ISSN 0014-5793. PMID 11094155.
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ignored (help) - ^ Walczak, H (1997). "TRAIL-R2: a novel apoptosis-mediating receptor for TRAIL". EMBO J. 16 (17). ENGLAND: 5386–97. doi:10.1093/emboj/16.17.5386. ISSN 0261-4189. PMC 1170170. PMID 9311998.
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ignored (help) - ^ Hymowitz, S G (1999). "Triggering cell death: the crystal structure of Apo2L/TRAIL in a complex with death receptor 5". Mol. Cell. 4 (4). UNITED STATES: 563–71. doi:10.1016/S1097-2765(00)80207-5. ISSN 1097-2765. PMID 10549288.
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ignored (help) - ^ a b MacFarlane, M (1997). "Identification and molecular cloning of two novel receptors for the cytotoxic ligand TRAIL". J. Biol. Chem. 272 (41). UNITED STATES: 25417–20. doi:10.1074/jbc.272.41.25417. ISSN 0021-9258. PMID 9325248.
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Further reading
External links
- TNFRSF10B+protein,+human at the U.S. National Library of Medicine Medical Subject Headings (MeSH)
This article incorporates text from the United States National Library of Medicine, which is in the public domain.