2008
DOI: 10.1038/cr.2008.277
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Negative feedback regulation of cellular antiviral signaling by RBCK1-mediated degradation of IRF3

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Cited by 134 publications
(97 citation statements)
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“…Several ubiquitin ligase enzymes have been identified to regulate these processes [28][29][30][31][32][33][34][35]. However, only a few DUBs are known to regulate these pathways: A20 was shown to negatively regulate the RIG-I-induced antiviral state [36], DUBA was identified to be required for efficient deubiquitination of TRAF3 and to function as a negative regulator of innate immune responses [25], and CYLD, known as a tumor suppressor, was recently reported to negatively regulate the activation of TBK1/ IKKε [37].…”
Section: Introductionmentioning
confidence: 99%
“…Several ubiquitin ligase enzymes have been identified to regulate these processes [28][29][30][31][32][33][34][35]. However, only a few DUBs are known to regulate these pathways: A20 was shown to negatively regulate the RIG-I-induced antiviral state [36], DUBA was identified to be required for efficient deubiquitination of TRAF3 and to function as a negative regulator of innate immune responses [25], and CYLD, known as a tumor suppressor, was recently reported to negatively regulate the activation of TBK1/ IKKε [37].…”
Section: Introductionmentioning
confidence: 99%
“…Similar to IRF3, virus infection induces C-terminal phosphorylation and activation of IRF7. Until now, many kinds of factors have been found to negatively regulate IRF3-dependent signaling (16)(17)(18)(19); however, the molecular mechanisms for the regulation of IRF7 remain to be further identified.…”
mentioning
confidence: 99%
“…Various molecules, including A20, DUBA, RNF125, Pin1, RBCK1, NLRX1, SIKE, DAK, and LGP2, have been shown to regulate induction of type I IFNs by targeting distinct components of the virus-triggered signaling pathways (26)(27)(28). In this report, we found that ISG56 was associated with the adapter protein MITA and disrupted the interaction of MITA with VISA or TBK1, leading to the inhibition of virus-induced IRF3 activation, IFN-␤ expression, and cellular antiviral responses.…”
mentioning
confidence: 99%