IndraLab
Statements
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"Indeed, our results demonstrate that upregulation of CYLD in cardiomyocytes impairs autophagy at the stage of autolysosome efflux and enhances myocardial death in PO-hearts."
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"Overexpression of CYLD promoted more apoptotic death ratio in PC-9/GR cells than that in PC-9 cells."
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"IKK blockade reactivates CYLD, as evidenced by the reduction in RIPK1 ubiquitination, which leads to the association of RIPK1 with the death-inducing signaling complex (DISC) to trigger cell death."
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"CYLD inactivates mechanistic target of rapamycin complex 1 (mTORC1) reactivation, upregulates Ras genes from rat brain 7 (Rab7) and enhances cardiomyocyte death in pressure overloaded hearts.."
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"Following the TNFR1 mediated assembly of pro inflammatory complex I, deubiquitinases (CYLD or A20) remove polyubiquitin chains from RIPK1 to terminate inflammation and enable downstream death signaling [50,51]."
| PMC
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"In addition, Cyld gene gain- and/or loss-of-function approaches in vitro and in vivo demonstrated that CYLD mediated cardiomyocyte death associated with impaired reactivation of mechanistic target of rapamycin complex 1 (mTORC1) and upregulated Ras genes from rat brain 7 (Rab7), two key components for autolysosomal degradation."
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"Nonetheless, it is possible for death-signaling CYLD and RIPK1 molecules, activated by disruption of the early checkpoint, to override the protection provided by the second NFκB-dependent checkpoint."