TRAIL receptor-2 signals apoptosis through FADD and caspase-8
By J. Bodmer, N. Holler, Sévérine Reynard, P. Vinciguerra, P. Schneider, P. Juo, J. Blenis, J. Tschopp. Nature Cell Biology, 2000
692 citations recorded by the source corpus.
Subfields: Immunology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/fa0ad4aa0b0753db1877449a168e3c62b9ef2563
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In Immunology
- A. Mantovani
- P. Allavena
- Alexandru Almasan
- G. Germano
- Heidi N. Leblanc
- A. Ashkenazi
- A. Sica
- F. Balkwill
In Molecular Biology
- Alexandru Almasan
- P. Allavena
- Heidi N. Leblanc
- A. Mantovani
- A. Ashkenazi
- Carlos M. Galmarini
- F. Balkwill
- M. Karin
Citations in the corpus
- Apo2L/TRAIL and its death and decoy receptors (2003, background): “Unlike the TNFR1 DISC, TRADD and RIP do not appear to be present in the native Apo2L/TRAIL DISC.28,29 Apo2L/TRAIL can trigger apoptosis independently through DR4 or DR5.”
- Role of macrophage targeting in the antitumor activity of trabectedin. (2013, background): “This caspase is the key effector molecule of the extrinsic apoptotic pathway mediated by membrane death receptors (Fas and tumor necrosis factor-related apoptosis inducing ligand [TRAIL] receptors [TRAIL-Rs]) (Bodmer et al., 2000).”
- Apo2L/TRAIL: apoptosis signaling, biology, and potential for cancer therapy. (2003, background): “In untransfected cells, the Apo2L/TRAIL DISC is similar to that of FasL, with the adaptor protein Fas-associated death domain (FADD, also called Mort-1 (Chapter by Genhong Chen; Reference—CGFR CHAPTER: cell death-death domain adaptors in signaling activated by TNF family)) and the apoptosis initiato”
- Mechanisms of resistance to TRAIL-induced apoptosis in cancer (2005, result): “The conclusions from this study, that FADD is essential in TRAIL-induced apoptosis and that dysfunction of FADD can cause TRAIL resistance, are also supported by another study that used Jurkat cells.(37) In that study, FADD-deficient Jurkat cells were resistant to TRAIL even at very high concentrati”
- Apoptosis and cancer: mutations within caspase genes (2009, background): “DISC signalling can be inhibited by expression of c-FLIP, a physiologic dominant negative caspase-8 that leads to the formation of a signalling inactive DISC.19 The intrinsic or mitochondrial pathway is activated by a variety of extra- and intracellular stresses, including oxidative stress, irradiat”