IndraLab

Statements


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eidos
"However , as viral infection goes on , CYLD accumulates and cleaves the K63-linked ubiquitin chains of RIG-I , inhibiting virus-triggered type I IFN signaling ."

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"Ectopic expression of CYLD antagonizes the IFN response whereas siRNA-mediated knockdown of CYLD expression allows for a more robust IFN response."

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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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"Several DUBs were shown to have an inhibitory effect on the RIG-I signalling pathway (Fig XREF_FIG), as for example knockdown of CYLD enhanced type-I IFN production in response to SeV infection whereas ectopic CYLD expression inhibited it XREF_BIBR."

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"Since CYLD negatively regulates IFN induction, XREF_BIBR, XREF_BIBR we examined whether the loss of CYLD renders mice more resistant to viral infection."

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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."

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"The deubiquitinating enzyme CYLD cleaves K63 linked polyubiquitin chains from specific substrates, including tumor necrosis factor receptor associated factors (TRAF)-2, TRAF6, transforming growth factor beta activated kinase 1 (TAK1), B cell lymphoma 3 (BCL3), STAT3, nuclear factor kappa B essential modulator (NEMO), and retinoic acid inducible gene 1 (RIG-1), and negatively regulates the activation of NF-kappaB, MAPKs, and type I IFN production."

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"Strikingly, the CYLD and TRAF3 genetic alterations affected mutually exclusive HPV+ HNSCC tumor groups, suggesting that alterations in either TRAF3 or CYLD may function independently and sufficiently to deregulate the downstream NF-kappaB and IFN responses."