IndraLab

Statements


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

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

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