IndraLab

Statements


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"SMAC mimetics can similarly disrupt CYLD phosphorylation and lead to ATLL cell death through reduction of RIPK1 ubiquitination, which is CYLD dependent."

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"Ablation of the RIP1 deubiquitinase CYLD largely blocked apoptotic and necroptotic cell death induced by TAK1 inhibition."

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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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"Conversely, CYLD inhibits cell death in certain contexts."

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"Lastly, CYLD inhibits pyroptosis, a pro-inflammatory form of cell death mediated by caspase-1 in response to lipopolysaccharide stimulation (Li et al., 2019)."

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"Consistent with the data above, silencing CYLD largely abolished caspase 8 activation and necroptotic cell death induced by 5z-7 plus TNFalpha (XREF_FIG)."

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"Our studies reveal that under physiological conditions, TNF- and RIPK1-dependent cell death is suppressed by the linear ubiquitin-dependent inhibition of CYLD."

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"However, prolonged ATRA treatment reduced CYLD SUMOylation and promoted cell death instead."

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"For example, in cultured endothelial cells, Cyld was upregulated; autophagosomes accumulated; and knockdown of Cyld or Atg7 similarly rescued cell death in a setting of autophagic flux by palmitic acid overloading [55]."

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"Despite SPATA2- or CYLD-deficient cells being less sensitive than their wild-type counterparts to various forms of TNF-induced cell death, SPATA2-deficient mice are actually more sensitive than wild-type mice to TNF toxicity."

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"In addition to CYLD, these kinases can also directly phosphorylate RIPK1 to inhibit cell death."

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"Limited evidence supports our contradictory findings, as the RIPK3-mediated death observed in the colon of intestinal epithelial NEMO deficiency was not rescued by Cyld DUB deficiency [40], while the repression of Cyld in neuronal cells promoted cell death but did not alter NF-κB activity upon brain injury [41]."

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"Therefore, decreased CYLD expression in RD rats may inhibit necroptotic cell death by increasing ubiquitination and inhibiting phosphorylation of RIP1."

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"First, individually KO of CYLD, caspase-8, and FADD (required for caspase-8 activation) in HeLa cells (Fig. 3 A) and KO of CYLD and caspase-8 in HCT-116 cells (Fig. 3 B) blocked TNF/IFNγ-induced cell death."