IndraLab

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CYLD activates Death. 11 / 11
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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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"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."
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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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"Collectively, the above results indicate that CYLD inactivation causes spontaneous hepatocyte death via prolonged activation of JNK."
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"As such, there is an urgent need to identify reliable predictive biomarkers and targeted therapeutic strategies for EC.Necroptosis is a form of programmed inflammatory cell death (7), mediated by MLKL, RIPK3, RIPK1, CYLD, cIAP1/2, and caspase-8 and inhibited by GSK843, GSK872, Nec-1, NSA, zVAD-fmk smac and other mimetics (7, 8)."
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"Our results expose CYLD as a mediator of necroptosis inducing RIP1/RIP3 complex formation in neurons in vitro and demonstrate a major role of such CYLD-mediated death pathways in acute brain injury in vivo.The discovery of a controlled signaling network regulating programmed necrosis dispensed the view that necrotic cell death always occurs in an uncontrolled manner [14]."
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"Similarly, knockdown CYLD in EMT6 cells and in murine BMDMs inhibited TNF/IFNγ-induced death (Fig. S4, A–D)."
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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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"These results reveal that CYLD is capable of mediating ROS formation via suppressing Nrf2 expression in cardiomyocytes.Because over produced ROS cause cardiomyocyte death and hypertrophy in various pa[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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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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