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Details on Person TRIF was repored to efficiently induce apoptosis when overex...

Class:Id	Summation:2584544
_displayName	TRIF was repored to efficiently induce apoptosis when overex...
_timestamp	2017-07-26 05:53:22
created	[InstanceEdit:2584543] Shamovsky, V, 2012-11-14
literatureReference	[LiteratureReference:936978] Apoptosis induced by the toll-like receptor adaptor TRIF is dependent on its receptor interacting protein homotypic interaction motif [LiteratureReference:2584548] Tipping the balance between necrosis and apoptosis in human and murine cells treated with interferon and dsRNA [LiteratureReference:2562571] dsRNA induces apoptosis through an atypical death complex associating TLR3 to caspase-8 [LiteratureReference:2584562] The Ripoptosome, a signaling platform that assembles in response to genotoxic stress and loss of IAPs [LiteratureReference:2562551] cIAPs block Ripoptosome formation, a RIP1/caspase-8 containing intracellular cell death complex differentially regulated by cFLIP isoforms
modified	[InstanceEdit:9013877] Shamovsky, Veronica, 2017-07-26
text	TRIF was repored to efficiently induce apoptosis when overexpressed in human HEK293T cells. TRIF-induced apoptosis occurred through activation of the FADD-caspase-8 axis (Kaiser WJ and Offermann MK 2005; Kalai M et al. 2002; Estornes Y et al. 2012). C-terminus of TRIF was shown to form complexes with both RIP1 and RIP3, and disruption of these interactions by mutating the RHIM eliminated the ability of TRIF to induce apoptosis (Kaiser WJ and Offermann MK 2005). Prevention of RIP1 ubiquitination leads to a strong association of RIP1 and caspase-8 (Feoktistova M et al. 2011, Tenev et al. 2011).
(summation)	[Reaction:2562541] TLR4-induced ripoptosome assembly [Homo sapiens]
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