IndraLab

Statements



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"We found that inhibition of cyld expression in Jurkat cells also attenuated necroptosis (XREF_FIG)."

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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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"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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"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, loss of CYLD in vivo was shown to delay, but not prevent necroptosis during skin inflammation [XREF_BIBR]."

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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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"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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"CYLD is required for TLR3 or TLR4 receptor induced necroptosis."

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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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"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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"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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"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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"Loss of CYLD would then prevent necroptosis and sustain cell survival."