The CD95(APO-1/Fas) DISC and beyond
By Marcus E. Peter, P. Krammer. Cell Death and Differentiation, 2003
1,176 citations recorded by the source corpus.
Subfields: Immunology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/dbabf0f52bfe556d38fa6443ed5202283197863b
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In Immunology
In Molecular Biology
- Peter Vandenabeele
- Zhaoyu Jin
- D. Lawrence
- Jennie Lill
- Yun Li
- Victoria C. Pham
- R. Pitti
- T. Vanden Berghe
Citations in the corpus
- MicroRNAs: key players in the immune system, differentiation, tumorigenesis and cell death (2008, background): “In the extrinsic apoptosis pathway, surface receptors of the death receptor family that include TNFRI, CD95 (Fas/APO-1) and the TNF-related apoptosis inducing ligand (TRAIL) receptors DR4 and DR5 (Schulze-Osthoff et al., 1998), once triggered by their cognate ligands, recruit adaptor proteins (FADD ”
- Cullin3-based polyubiquitination and p62-dependent aggregation of caspase-8 mediate extrinsic apoptosis signaling. (2009, positive): “In ‘‘type II’’ cells, further signal amplification is required; this occurs by caspase-8-mediated processing of the Bcl-2 homology domain 3 protein Bid, which engages the mitochondria to promote further caspase activation (Peter and Krammer, 2003).”
- Receptor interacting protein kinase-3 determines cellular necrotic response to TNF-alpha. (2009, background): “…of various death-inducing cytokines including TNF-a, TRAIL, and CD95 ligand to their respective receptors leading to the activation of caspase-8 (Peter and Krammer, 2003); The intrinsic pathway is activated after mitochondrial intermembrane space proteins such as cytochrome c and Smac/Diablo…”
- Necrosis, a well-orchestrated form of cell demise: signalling cascades, important mediators and concomitant immune response. (2006, background): “When they bind their extracellular ligands they aggregate and initiate a signalling pathway that results either in cell survival or in death [27].”
- Caspases in cell survival, proliferation and differentiation (2007, background): “In contrast, caspase-8 processing and strong activation is seen during FasL-induced apoptosis (Figure 1a).(4) An important player in the regulation of caspase-8 activation at the level of the DISC is c-FLIPL, a caspase-8-like molecule that lacks caspase activity.”