IndraLab

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USP18 activates IFNA. 21 / 21
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"In the current study, for the first time, we demonstrated that ISG15 and USP18 protein levels are increased in HCV infected PHHs and IFN-lambda4-expressing or -treated cells and that ISG15 and USP18 proteins mediate IFN-alpha unresponsiveness in IFN-lambda4-expressing or -treated cells."
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"Taken together, we concluded that USP18 potentiates the anti-HBV activity of IFN-alpha by targeting the JAK and STAT signaling pathway in Hepg2.2.15 cells."
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"Furthermore, previous studies reported that blocking of IFN-α signaling by USP18 does not depend on the enzymatic activity of USP1827."
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"Usp18 deficient cells have enhanced IFN-alpha and beta signaling and more ISG15 modified proteins."
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"Our results indicated that USP18 modulates the anti-HBV activity of IFN-alpha via activation of the JAK and STAT signaling pathway in Hepg2.2.15 cells."
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"For example, ischemic reperfusion injury upregulates USP18 expression in the liver and induces an IFN-α refractory state."
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"In the absence of ISG15, USP18 proteolysis is more rapid, driving the dysregulated IFN-alpha and beta response and resulting in both the blood IFN-alpha and beta signature and brain calcifications seen in the patients."
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"Furthermore, previous studies reported that blocking of IFN-alpha signaling by USP18 does not depend on the enzymatic activity of USP18 27."
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"Treatment of Huh7.5 cells and primary murine hepatocytes with LPS and TNF-α, but not IL-6 or IL-10, led to upregulated USP18 expression and induced an IFN-α refractory state, which was reversed by USP18 knockdown."
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"The IFN-alpha signal blocking activity of USP18 is mediated by the binding of USP18 to the intracellular domain of IFNAR2, which prevents the binding of JAK1 to IFNAR2 27."
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"In addition, lacking USP18 can abrogated the refractory status induced by IFN-alpha stimulation, which indicates that lack of USP18 in the Hepg2.2.15 cells could enhance the antiviral activity of IFN-alpha (XREF_SUPPLEMENTARY)."
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"Leading edge analysis showed that, as compared to treated cells, untreated cells were enriched in NF‐κB pathway genes but ‘IFNA response’ genes including type I IFN genes ISG15, IFIT2, IFIT3, MX1 and USP18 41 were induced by DMX3433 treatment.4 DISCUSSION."
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"Namely, free extracellular ISG15 is crucial in IFN-gamma-dependent antimycobacterial immunity, while free intracellular ISG15 is crucial for USP18 mediated downregulation of IFN-alpha and beta signalling."
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"The ISG15 and USP18 mediated IFN-alpha unresponsiveness was demonstrated by transfection of siRNAs targeting ISG15 and/or USP18."
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"The ISG15/USP18-mediated IFN-α unresponsiveness was demonstrated by transfection of siRNAs targeting ISG15 and/or USP18."
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"The IFN-α signal-blocking activity of USP18 is mediated by the binding of USP18 to the intracellular domain of IFNAR2, which prevents the binding of JAK1 to IFNAR2 27 ."
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"The IFN-α signal-blocking activity of USP18 is mediated by the binding of USP18 to the intracellular domain of IFNAR2, which prevents the binding of JAK1 to IFNAR227.Our group recently found that prolonged stimulation of IFN-λ3 induces the robust and sustained upregulation of ISG15 that stabilizes the USP18 protein and causes the unresponsiveness to exogenous IFN-α treatment10."
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"In cell culture, siRNA mediated depletion of USP18 enhanced ISG induction as well as the antiviral effect of IFN-alpha against HCV replication."
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"Treatment of Huh7.5 cells and primary murine hepatocytes with LPS and TNF-alpha, but not IL-6 or IL-10, led to upregulated USP18 expression and induced an IFN-alpha refractory state, which was reversed by USP18 knockdown."
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"Error bars represent the SEM for duplicate PCRs.FIG 4: ISG15 deubiquitination does not play a role in USP18-mediated IFN-α refractoriness."
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"These results collectively suggested that silencing USP18 activated IFN-alpha signaling, JAK and STAT signaling, in a prolonged fashion."
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