The Ripoptosome, a signaling platform that assembles in response to genotoxic stress and loss of IAPs.

By T. Tenev, K. Bianchi, M. Darding, Meike Broemer, C. Langlais, Fredrik Wållberg, A. Zachariou, Juanita Lopez, M. MacFarlane, K. Cain and 1 more. Molecules and Cells, 2011

852 citations recorded by the source corpus.

Subfields: Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/6a2ff2d1dc7a0d023f00f7953f4421d6e6626b5b

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

In Physiology

Citations in the corpus

Cell Death Signaling. (2015, background): “Finally, DNA damage signaling can also cause RIPoptosome formation independently of any membrane receptor signaling (Tenev et al. 2011).”
Caspases in Cell Death, Inflammation, and Gasdermin-Induced Pyroptosis (2020, background): “However, recruitment of cFLIP to the ripoptosome complex diverts the apoptotic activity of caspase-8 to prosurvival inflammatory signaling (1, 21, 25, 56, 57).”
Caspase-8 induces cleavage of gasdermin D to elicit pyroptosis during Yersinia infection (2018, background): “In mouse macrophages, complex IIa forms when there are inadequate prosurvival factors, including cellular FLICE-inhibitory protein (cFLIP) (57) and inhibitors of apoptosis (IAPs) (25).”
Regulation of tumour necrosis factor signalling: live or let die (2015, background): “Enforced FLIP L expression prevents the assembly of complex IIb, whereas overexpression of FLIP S (and potentially that of the closely related FLIP R ) facilitates complex IIb formation 71,91 .”
From pyroptosis, apoptosis and necroptosis to PANoptosis: A mechanistic compendium of programmed cell death pathways (2021, background): “CASP8 and the kinase activity of RIPK1 are essential for ripoptosome-induced apoptosis and necroptosis, respectively [125].”
Caspases and their substrates (2017, background): “the formation of the necroptosome, formed by RIPK1, RIPK3, FADD, cFLIP, and caspase-8.(83,84) The mechanism by which”
Toll-like receptors activate programmed necrosis in macrophages through a receptor-interacting kinase-3–mediated pathway (2011, background): “Recently, two independent groups have demonstrated that a cytosolic complex named Ripoptosome containing RIP1, FADD, caspase 8, and cFLIP, was formed upon IAP degradation and induced both apoptosis and necrosis (26, 27).”
DAI complexes with RIP3 to mediate virus-induced programmed necrosis that is targeted by murine cytomegalovirus vIRA (2012, positive): “Recent work showing the role of the “Ripoptosome” signaling platform in necroptosis (Feoktistova et al., 2011; Tenev et al., 2011) suggests that a DAIRIP3 complex may engage or coordinate a similar signaling platform to execute virusinduced programmed necrosis.”
The RIP1/RIP3 Necrosome Forms a Functional Amyloid Signaling Complex Required for Programmed Necrosis (2012, neutral): “Active caspase-8 within the Ripoptosome cleaves and inactivates RIP1 (Chan et al., 2003; Lin et al., 1999) and RIP3 (Feng et al., 2007).”