IndraLab

Statements



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"In this study, we used transgenic mouse and human SCC models to investigate how CYLD loss-of-function leads to abnormal signal transduction and promotes tumorigenesis."

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"CYLD is a deubiquitination enzyme targeting lysine 63 linked ubiquitin chains and was shown to negatively regulate signal transduction factors and pathways including transforming growth factor-beta and NF-kappaB signaling pathways [XREF_BIBR - XREF_BIBR]."

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"As both CYLD and OTULIN negatively regulate the NF-kappaB signalling cascade, the impact of these deubiquitinases in different LUBAC dependent signalling cascades may be context dependent."

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"It has been proposed that CYLD inhibits proinflammatory signal transduction [23,35] ."

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"These findings suggest that CYLD can both positively and negatively regulate signal transduction and homeostasis of B cells in vivo, depending on the expression of CYLD splice variants."

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"Because of abnormal activation of NF-kappaB, CYLD deficiency attenuates the signal transduction of NKT cells stimulated by IL-7."

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"For example, CYLD removes polyubiquitin chains from TBK1 and RIG-I and thus inhibits the IRF3 signaling pathway and IFN production triggered by RIG-I; conversely, CYLD knockdown enhances this response (58)."

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"Ectopic expression of CYLD inhibits the IRF3 signalling pathway and IFN production triggered by RIG-I; conversely, CYLD knockdown enhances the response."