The apoptosome: signalling platform of cell death

By S. Riedl, G. Salvesen. Nature reviews. Molecular cell biology, 2007

1,155 citations recorded by the source corpus.

Subfields: Epidemiology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/a8ee886ed3be4adfce90ce7532e28cf8b9e46199

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Citations in the corpus

Inflammasomes and their roles in health and disease. (2012, background): “…viewpoint because the large prodomains of initiator caspases typically contain interaction motifs of the death domain superfamily that allow recruitment of the zymogen into activating protein complexes such as the inflammasome and the apoptosome (Lamkanfi & Dixit 2009, Riedl & Salvesen 2007).”
The BCL-2 Family Reunion (2010, background): “The caspases cleave cellular substrates to elicit the apoptotic phenotype (Figure 1A) (Riedl and Salvesen, 2007).”
Role of Bcl-2 family proteins and caspases in the regulation of apoptosis (2011, background): “The cyt c plays the main role in this pathway which is activated after its interaction with apoptotic protease-activating factor (Apaf1) and deoxyadenosine triphosphate (dATP) to form apoptosome [102, 105].”
Crosstalk between apoptosis, necrosis and autophagy. (2013, background): “This binds and promotes the activation of initiator caspase-9, which then activates executioner caspases-3 and -7 that cleave several substrates to elicit the apoptotic phenotype [62].”
Analysis of mitochondrial function in situ in permeabilized muscle fibers, tissues and cells (2008, background): “Recently, mitochondria are being considered an integral part of multiple cellular signaling cascade”
Apoptotic caspases prevent the induction of type I interferons by mitochondrial DNA (2014, background): “Together with Apaf-1 and caspase-9, cytosolic cytochrome c forms a protein complex called the apoptosome, which induces the activation of caspase-9 (Jiang and Wang, 2004; Riedl and Salvesen, 2007).”
Cullin3-based polyubiquitination and p62-dependent aggregation of caspase-8 mediate extrinsic apoptosis signaling. (2009, neutral): “In the intrinsic pathway, the ‘‘apoptosome’’ mediates multimerization of the apical protease caspase-9, facilitating its full activation (Jiang and Wang, 2004; Riedl and Salvesen, 2007).”
How do BCL-2 proteins induce mitochondrial outer membrane permeabilization? (2008, neutral): “DNA laddering, nuclear condensation, and cellular blebbing; for more information, refer to [ 2 ]).”
Cytochrome c: functions beyond respiration (2008, background): “In vertebrates, caspase-dependent apoptosis occurs through two main pathways: the extrinsic pathway and the intrinsic pathway”
Lysosomal membrane permeabilization in cell death (2008, background): “This complex, which is composed of cytochrome c as well as Apaf-1, results in the recruitment and allosteric activation of caspase-9, which then activates caspase-3 (Riedl and Salvesen, 2007).”
Reactive Oxygen Species-Induced Lipid Peroxidation in Apoptosis, Autophagy, and Ferroptosis (2019, background): “An assembly of apoptosome leads to caspase-9 activation, which further activates caspase-3, for apoptotic execution [58].”
The inflammasome: an integrated view (2011, background): “The apoptosome, which was described many years before the inflammasome, is an APAF1- and caspase-9-containing protein complex that is induced by various stress conditions and initiates programmed cell death (71).”