IndraLab

Statements


USP18 inhibits IFNA. 25 / 26
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"We speculate that by blocking IFN-alpha signaling, USP18 expression may lead to an enhanced susceptibility to infection with interferon sensitive viruses and enhanced viral proliferation."

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"Lack of USP18 was shown to abrogate this desensitizing effect of IFN-alpha in vivo [XREF_BIBR], whereas USP18 expression was sufficient to establish this state of refractoriness [XREF_BIBR]."

sparser
"The reason for this paradox is unknown, but IFN-λ4 has been speculated to render HCV-infected hepatocytes refractory to IFN-α, for example by inducing the expression of USP18, which inhibits IFN-α but not IFN-λ signaling41."

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"The reason for this paradox is unknown, but IFN-lambda4 has been speculated to render HCV infected hepatocytes refractory to IFN-alpha, for example by inducing the expression of USP18, which inhibits IFN-alpha but not IFN-lambda signaling XREF_BIBR."

eidos
"USP18 , downregulates the production of IFNalpha through interaction with IFNAR signaling [ 326 ] ."
| PMC

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"Further proviral ISG15 functions stem from human ISG15 interactions, which are crucial for USP18 mediated inhibition of IFN-alpha and beta signaling responses."

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"However, knockdown of USP18 reversed this effect and augmented the effect of IFN-α (Fig. 3B, columns 9, 10, 12, and 14)."

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"USP18 inhibition by two independent siRNAs increased beta cell apoptosis following exposure to IFNalpha or IFNgamma (XREF_FIG), whereas siCTRL has no such effect."

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"The reason for this paradox is unknown, but IFN-λ4 has been speculated to render HCV-infected hepatocytes refractory to IFN-α, for example by inducing the expression of USP18, which inhibits IFN-α but not IFN-λ signaling41."

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"In hepatoma cells, IFNL4 gene transfection or recombinant IFN-lambda4 protein treatment robustly increased the protein levels of ISG15 and USP18 in an IFNLR1 dependent manner and potently blocked IFN-alpha signalling."

eidos
"IFN-lambda4 potently blocks IFN-alpha signalling by ISG15 and USP18 in hepatitis C virus infection ."

eidos
"The reason for this paradox is unknown , but IFN-lambda4 has been speculated to render HCV-infected hepatocytes refractory to IFN-alpha , for example by inducing the expression of USP18 , which inhibits IFN-alpha but not IFN-lambda signaling41 ."

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"The results suggested that USP18 silencing augments the antiviral effects of IFN-alpha against HBV expression (XREF_FIG)."

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"Studies from ours and others demonstrated that higher expression levels of USP18 inhibited IFN-a anti-HBV and HCV activity in chronic HBV- and HCV infected patients [XREF_BIBR, XREF_BIBR]."

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"USP18 silencing enhances the antiviral activity of IFN-alpha through JAK-STAT signaling pathway."

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"Of note, USP18 knockdown did not increase pSTAT1 in response to IFN-alpha before 24 h; these findings are consistent with previous observations."

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"Next, we determined whether USP18 silencing enhances the antiviral activity of IFN-alpha against HBV."

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"However, knockdown of USP18 reversed this effect and augmented the effect of IFN-alpha (XREF_FIG, columns 9, 10, 12, and 14)."

eidos
"IFN-lambda4 potently blocks IFN-alpha signalling by ISG15 and USP18 in hepatitis C virus infection OPEN ."

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"In hepatoma cells, IFNL4 gene transfection or recombinant IFN-λ4 protein treatment robustly increased the protein levels of ISG15 and USP18 in an IFNLR1-dependent manner and potently blocked IFN-α signalling."

eidos
"However , knockdown of USP18 reversed this effect and augmented the effect of IFN-alpha ( Fig. 3B , columns 9 , 10 , 12 , and 14 ) ."

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"This desensitizing effect indicates that lack of USP18 in the Hepg2.2.15 cells could abrogate this desensitizing effect of IFN-alpha and enhance the antiviral activity of IFN-alpha."

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"Silence of USP18 potentiated the anti-DENV-2 activity of IFN-alpha through activation of the IFN-alpha-mediated Jak and STAT signaling pathway as shown by increased expression of p-STAT1 and p-STAT2, enhanced ISRE activity, and elevated expression of some ISGs."

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"We speculate that by blocking IFN-α signaling, USP18 expression may lead to an enhanced susceptibility to infection with interferon-sensitive viruses and enhanced viral proliferation."

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"Moreover, USP18 competitively inhibits IFN-alpha and beta-induced JAK and STAT activation [XREF_BIBR] and upregulates epidermal growth factor receptor (EGFR) expression [XREF_BIBR]."