IndraLab

Statements

CYLD activates cell death. 26 / 29
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"Genetic manipulation of Cyld in combination with pharmacological modulation of autophagic functional status revealed that CYLD suppressed autolysosomal degradation and promoted cell death in cardiomyocytes."
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"CYLD can limit TNF-induced prosurvival signaling and promote cell death [ 76 ] [ 77 ] [ 78 ] ."
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"CYLD can limit TNF-induced prosurvival signaling and promote cell death [ 76-78 ] ."
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"In control non targeting siRNA transfected cells, the treatment with TNFalpha induced at least 60-70% cell death, which is blocked by knockdown of cyld and tnfr1 but not by that of rip1 (XREF_FIG)."
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"We have detected that overexpression of CYLD contributed to cell death of the lung cancer cells."
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"Increasing CYLD promotes apoptosis and increasing PNUTL enhances cell death via TGF."
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"A genome-wide siRNA screen linked CYLD to receptor interacting protein-1 (RIP1) kinase mediated necroptosis; however, the exact mechanisms of CYLD mediated cell death remain unknown."
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"However, more importantly, five recently published reports have highlighted that SPATA2 is crucial for recruiting CYLD to the TNFR1 signaling complex thus promoting its activation leading to TNF-induced cell death."
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"All of the results demonstrated that overexpression of CYLD promoted cell death and CYLD played an antitumor activity in the human lung cancer cells."
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"These findings unravel the mechanisms of CYLD mediated cell death signaling in damaged neurons in vitro and suggest a cell death mediating role of CYLD in vivo."
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"The tumor suppressor cylindromatosis (CYLD), which promotes RIPK1-dependent cell death, is also controlled by inhibitory phosphorylation by the IKK and TBK1 kinases [45]."
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"Taken together, these results indicate that CYLD can promote autophagy inhibition-induced cell death most likely via suppressing autolysosome efflux in cardiomyocytes."
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"21 Previously, it was reported that CYLD promotes induction of cell death by TNF-alpha."
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"XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR In cell death assays, overexpression of CYLD significantly enhanced induction of cell death stimulated by TNF-alpha, but this effect was abolished in CLIPR-59 knock-down cells (XREF_FIG)."
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"Immune dysregulation in SHARPIN-deficient mice is dependent on CYLD-mediated cell death."
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"Genetic manipulation of Cyld in combination with pharmacological modulation of autophagic functional status revealed that CYLD suppressed autolysosomal degradation and promoted cell death in cardiomyocytes ."
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"We showed that CYLD dependent RIPK1 and RIPK3 necrosome formation occurred in neuronal cells exposed to ferroptosis activators and knockdown of the necroptosis-mediators CYLD, RIPK1 or RIPK3 attenuated cell death."
| PMC
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"Because not the basal but BafA1-induced cell death in MEF was inhibited by knockdown of CYLD (Fig. 6E), it is likely that CYLD mediates cell death in stressed cardiomyocytes via suppressing autophagy at the stage of autolysosome efflux."
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"CYLD Limits Gene Activation and Enhances Cell Death in Response to TNF."
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"Firstly, we asked whether overexpression of CYLD-flag could induce cell apoptosis, which probably contributed to CYLD induced cell death."
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"Cell death initiated by TNF in Cyld -/- MEFs expressing CYLD-D215A was blocked by the RIPK1 inhibitor Necrostatin-1 17 (XREF_FIG, compare panel 6 and panel 7), or by specific knockdown of Ripk1 or Ripk3 (XREF_FIG), demonstrating that RIPK1 and RIPK3 are downstream of CYLD."
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"IKK blockade reactivated CYLD, as evidenced by the reduction in RIPK1 ubiquitination, which led to the association of RIPK1 with the DISC, triggering cell death."
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"CYLD can limit TNF induced prosurvival signaling and promote cell death [XREF_BIBR - XREF_BIBR]."
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"39 Thus, repression of CYLD may prevent cell death at the level of both TAK1 and RIP1."
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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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"Otherwise overexpression of CYLD induced TNF-alpha-induced cell death in A549 cells and H460 cells."
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