Induction of TNF receptor I-mediated apoptosis via two sequential signaling complexes.

By O. Micheau, J. Tschopp. Cell, 2003

2,732 citations recorded by the source corpus.

Subfields: Cancer Research, Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/77c467221b9ac15822a9b96b66cfe30d036ff849

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Citations in the corpus

Death by TNF: a road to inflammation (2022, background): “How TNFR1 signalling further evolves to induce cell death is less clear, but it requires the assembly of a secondary cytosolic complex, termed ‘complex II’, which originates from the binding of FAS-associated death domain-containing protein (FADD) to the receptor-dissociated complex I components TRA”
Signaling in innate immunity and inflammation. (2012, background): “The TNF-RI-associated signaling complex formed in response to TNF is transient as TRADD, RIP1, and TRAF2 shift to the cytoplasm to form what is referred to as complex II (Micheau and Tschopp 2003).”
Crosstalk in NF-κB signaling pathways (2011, background): “Whereas the membrane-associated complex I comprises TRADD, RIP1 and TRAF2 and is responsible for rapid NF-κB dependent expression of genes encoding antiapoptotic molecules, the cytosolic complex II, consisting of TRADD, RIP1, TRAF2, FADD, caspase-8 and caspase-10, is proapoptoti”
A guide to cell death pathways (2023, neutral): “The intracellular DD of activated TNFR1 recruits the DD-containing adaptor protein TRADD and RIPK1, a DD-containing kinase 32,33 (Fig.”
RNA recognition and signal transduction by RIG‐I‐like receptors (2009, background): “This observation is closely related to TNFR-mediated signaling, which is known to form a similar signaling complex (85); however, it remains unknown why IRF-3 is selectively activated by the IPS-1-containting signaling complex but not in TNFR-mediated signaling.”
Caspase-8 induces cleavage of gasdermin D to elicit pyroptosis during Yersinia infection (2018, background): “However, RIP1 also has a role in TNF-driven apoptosis via the formation of complex II (6).”
The Ripoptosome, a signaling platform that assembles in response to genotoxic stress and loss of IAPs. (2011, methodology): “Since the formation of this RIP1/FADD/caspase-8 complex occurs independently of death ligands, it cannot constitute complex-II, which per definition originates from complex-I (Micheau and Tschopp, 2003; Wang et al., 2008).”
Microglia and neurodegeneration: The role of systemic inflammation (2013, background): “The TNF p55 receptor forms a complex containing TNF receptor associated death domain (TRADD), which can dissociate and recruit FADD (FAS-associated via death domain) and caspase-8 to initiate apoptosis (Micheau and Tschopp, 2003).”
Autophagy, ferroptosis, pyroptosis, and necroptosis in tumor immunotherapy (2022, background): “The conversion of Complex I into Complex II is facilitated by deubiquitination of RIPK1 by cylindromatosis (CYLD).(142) When CASP8 is activated in complex II, apoptosis is initiated.”
From pyroptosis, apoptosis and necroptosis to PANoptosis: A mechanistic compendium of programmed cell death pathways (2021, background): “DISC is assembled by death receptor engagement, where DD-containing death receptors (e.g., Fas) and a DD-containing adaptor protein (e.g., FADD) interact [123,124].”