IndraLab

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CYLD activates necroptotic process. 21 / 21
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"CYLD can also mediate necroptosis independently of TNF receptors via TLR3 and TLR4 (Schworer et al., 2014) or via RIG-1 (Schock et al., 2017), and can mediate necroptosis-like cell death in response to oxidative stress in neuronal cells (Ganjam et al., 2018)."
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"42 It was also demonstrated that CYLD promotes necroptosis after deubiquitination of RIP1 in necrosomes."
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"Hyperactivation of CYLD may result in phosphorylation and activation of complex II to initiate necroptosis while inhibits apoptosis [10,67–72] ."
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"Specifically, CYLD removed lysine 63 and linear ubiquitin chains from RIP1 and promoted necroptosis in TNF receptor signaling, which was involved in the regulation of different cellular processes including inflammation, fibrosis, and cancer."
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"However, the sensitivities to A20 and CYLD are reversed in their effects on TTD as compared with mode 1, i.e., A20 counterintuitively inhibits necroptosis, while CYLD promotes necroptosis, as expected."
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"In addition, CYLD promoted necroptosis via interacting with RIP1 [26]."
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"Knockdown of the RNA sensing molecule RIG-I or the RIP1 deubiquitin protein, CYLD, but not STING, rescued cells from SeV induced necroptosis."
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"10 Active Caspase-8 not only initiates the apoptotic program but also cleaves and inactivates essential necroptosis mediators such as RIPK1, RIPK3 and CYLD."
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"We found that inhibition of cyld expression in Jurkat cells also attenuated necroptosis (XREF_FIG)."
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"Loss of CYLD would then prevent necroptosis and sustain cell survival."
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"As a consequence of inhibiting RIPK1 ubiquitylation, the requirement of CYLD to initiate necroptosis was greatly reduced, and therefore, we moved to an MLKL dependent model (data not shown)."
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"The cell death is suppressed by knockdown of CYLD or RIP1 or RIP3 or MLKL, suggesting that this necrosis is necroptosis and mediated by CYLD-RIP1-RIP3-MLKL signaling pathway."
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"Therefore, our data provides qualified support for the notion that Mtb infected macrophages, in vitro and in vivo, may be primed to undergo necroptotic death, with the exception of our finding that CYLD protein levels were strongly suppressed which, according to recent reports, impedes the induction of necroptosis."
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"Knockdown of CYLD reduced necroptosis as expected (28) (SI Appendix, Fig. S1H), suggesting siRNA oligos targeting CYLD worked well."
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"Based on in vitro studies, CYLD was proposed to promote necroptosis by removing ubiquitin chains from RIP1 and in this way facilitating the formation of the RIP1 and RIP3 containing “necrosome” comple[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"The deubiquitinase CYLD has been identified to be involved in TLR induced necroptosis in macrophages from wild derived MOLF mice."
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"It has previously been shown that knockout of lysine 63 deubiquitinase CYLD significantly inhibits necroptosis in other cell lines, and serum response factor (SRF) could regulate CYLD gene expression through p38 mitogen activated protein kinase (p38 MAPK)."
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"However, loss of CYLD in vivo was shown to delay, but not prevent necroptosis during skin inflammation [XREF_BIBR]."
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"CYLD is required for TLR3 or TLR4 receptor induced necroptosis."
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"CYLD deficient cells are protected from RIPK1 mediated necroptosis in response to TNF plus caspase inhibition with or without Smac mimetic."
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"Active caspase 8 in Complex IIa not only initiates the caspase cascade and the apoptotic program, but also cleaves and inactivates essential necroptosis mediators such as RIPK1, RIPK3 and CYLD."
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