Apo2L/TRAIL-dependent recruitment of endogenous FADD and caspase-8 to death receptors 4 and 5.

By F. Kischkel, David A. Lawrence, A. Chuntharapai, P. Schow, K. Kim, A. Ashkenazi. Immunity, 2000

1,005 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/d356090905560f87277ffb23c0a0269e852cd525

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Citations in the corpus

CD95's deadly mission in the immune system (2000, background): “Signalling by other death receptors Signalling of apoptosis by other members of the death receptor subfamily seems to follow the same basic rules and is initiated by the same sequential step”
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.”
From bench to clinic with apoptosis-based therapeutic agents (2000, background): “The signal transduction pathways for the two pro-apoptotic TRAIL receptors (DR4/TRAIL-R1 and DR5/TRAIL-R2/Apo-2/TRICK2/Killer) also seems to use both FADD and procaspase-8 in keeping with their molecular brethre”
The E-Cadherin and N-Cadherin Switch in Epithelial-to-Mesenchymal Transition: Signaling, Therapeutic Implications, and Challenges (2019, background): “Ligated death receptor (DR) 4 and DR5 attach to Fas-associated death domain (FADD) then caspase-8 to become a death-inducing signaling complex (DISC) [70,71].”
Proteases for Cell Suicide: Functions and Regulation of Caspases (2000, background): “Cells from FADD2/2 or Casp82/2 animals show complete resistance to at least three death receptors but have normal sensitivity to UV, DNA-damaging agents, and oncogenes (Table 2).”
Cullin3-based polyubiquitination and p62-dependent aggregation of caspase-8 mediate extrinsic apoptosis signaling. (2009, positive): “As previously established, ligand binding induces receptor clustering and recruitment of FADD and caspase-8, forming an apical DISC (Kischkel et al., 2000; Sprick et al., 2000).”
Necrosis, a well-orchestrated form of cell demise: signalling cascades, important mediators and concomitant immune response. (2006, background): “At the plasma membrane, formation of complex I, which consists of TNF-R1, TRAF2 and RIP1, leads to rapid activation of NF-κB [38,39] and MAPKs, such as p38 MAPK, JNK and ERK [21,40].”