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Interferon activates USP18. 48 / 56
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"Finally, we assessed IFN induced USP18 accumulation in cells silenced for SKP2."
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"Model fitting results and the parameter analysis.Pulsatile IFN-a treatment induces higher ISG expression in single cells.Heterogeneous delays in USP18 upregulation by IFN were observed in single cells."
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"The increased expression of dsRNA receptor TLR3 and IFN induced genes ISG56, ISG43, Mx1 and IFIT3 after stimulation with poly I : C mimicking a viral infection indicates that these cell lines can be used as effective in vitro models to study the bat 's innate immune responses to virus infection XREF_BIBR, XREF_BIBR."
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"ISG15 is removed from substrates by interferon-induced ubiquitin-specific peptidase 18 or severe acute respiratory syndrome coronavirus 2‒derived papain-like protease."
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"USP18 protein accumulated with similar kinetics in cells treated with IFN beta or IFN lambda1, reaching maximum level between 8 and 16 hr of stimulation (XREF_FIG)."
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"These IFN system genes include the dsRNA signal sensing factor TLR3, IFN, IFN signal transduction factor STAT1, IFN regulatory factor IRF7, putative IFN antiviral effectors Mx1, Mx2, PKR like, Viperin, IFI56, and other IFN stimulated genes (ISGs) IFI58, ISG15-1, ISG15-2, USP18, Gig1 and Gig2."
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"Such increased expression is likely due to the enhanced type I IFN signaling in Usp18 Ity9 mice since ISG15 is a well-known IFN inducible gene."
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"IFNAR2 (part of the type I IFN receptor complex (Fig. 2)) interacts directly with the IFN-induced protein Usp18, which inhibits the response to IFN-α10 but not to IFN-β or IFN-λ11,12, thereby creating, at least in human cells, a negative feedback loop for IFN-α."
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"The in vitro IFN induced USP18 mRNA change (USP18 IFN -N) was measured via comparison of quantitative PCR determined USP18 transcription levels of BPMCs cultured with and without IFN stimulation."
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"Given that type I IFN has been shown to induce IL-10 in a STAT1 dependent manner,, we examined whether the increase in type I IFN signaling in Usp18 Ity9 mice affected IL-10 production."
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"mCMV infection increased expression of representative IFN stimulated genes (IFIT3, OAS, LMP2, TGTP, and USP18) in both neonatal and adult brains to similarly large degrees."
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"USP18 is promptly induced by viral infection and IFN signaling [46]."
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"Additionally , Usp18 has been characterized in various species and demonstrated to possess interferon-sensitive response elements ( ISREs ) in its promoter region and to be strongly induced by type I IFNs [ 32,33,37 ] ."
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"In the present study, we have analyzed the genes directly regulated in post-IFN-alpha receptor signaling and found that intraperitoneal administration of mouse IFN-alpha, but not human IFN-alpha, activated expression of several prototypic IFN stimulated genes (ISGs), in particular signal transducers and activators of transcription (STAT1), IFN induced 15 kDa protein (ISG15), ubiquitin specific proteinase 18 (USP18) and guanylate binding protein 3 (GBP3) in the brain."
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"Firstly, like ISG15 itself, the predominant ISG15 conjugation and deconjugation enzymes UbE1L, UbcH8/UbcM8, HERC5/HERC6, and UBP43/USP18 are all induced by type I IFN stimulation."
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"Since USP18 is also induced by IFN, we tried to dissociate the individual contribution of USP18 and ISG15, using RNA interference."
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"As shown in Fig. 4 B, anti-IFN alpha/beta antibodies significantly reduced expression of the interferon stimulated genes ISG15 and USP18."
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"In contrast, in those cells that progressed beyond this phase, the IFN treatment could not initiate USP18 induction until the next cell cycle, resulting in extended delay times proportional to the times needed to reach the next cell cycle (XREF_FIG)."
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"On the other hand, higher levels of type I interferon may increase the expression of these negative regulators: recruitment of USP18 to the type I interferon receptor IFNAR desensitizes cells to any additional IFN-activating stimuli (96, 97), while increased SOCS1 expression suppresses responses to pathogens that activate interferon-pathway signaling like LPS (98)."
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"The expression of USP18 is strongly induced by type I and type III interferons [ 2 ] [ 3 ] [ 4 ] [ 5 ] , by the Toll-like receptor ( TLR ) agonists LPS [ 6 ] [ 7 ] [ 8] and polyI :C [ 6 ] ( synthetic analogy of dsRNA ) and by TNFalpha [ 7 ] ."
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"USP18 is promptly induced by viral infection and IFN signaling [XREF_BIBR]."
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"We find that interfering with IFN-I signaling pathway in infected patients, notably by targeting the interferon stimulated gene USP18, resulted in reduced PTEN expression similar to those observed in uninfected control donors."
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"Several reports by our group and others have supported the observation that RNase L modulates the stability of certain cellular mRNAs in the absence of viral infections, such as the RNA binding protein ELAVL1 (HuR), the double-strand RNA (dsRNA)-dependent protein kinase (PKR), the muscle differentiation transcriptional factor (MyoD), and the IFN stimulated genes 43 (ISG43) transcript."
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"For example, hepatic mRNA expression of IFN stimulated genes (ISGs, such as ISG15, OAS, IFI, IP10, and viperin) and IFN related pathway genes (MX and USP18) correlate with responses to peg-IFNalpha and RBV combination therapy for CH-C XREF_BIBR - XREF_BIBR."
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"USP18 , a protein of 368 aa in length and an ISG15 isopeptidase , is a negative regulator of type I and III IFN-activated JAK / STAT signaling [ 142 ] , and is rapidly upregulated by viral infection and IFNs ."
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"IFNAR2 (part of the type I IFN receptor complex (Fig. 2)) interacts directly with the IFN-induced protein Usp18, which inhibits the response to IFN-α but not to IFN-β or IFN-λ , thereby creating, at least in human cells, a negative feedback loop for IFN-α."
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"Previous studies demonstrated that USP18 can be induced by viral infections and IFN treatment, suggesting that USP18 may play a critical role in inflammation and host innate immune response [XREF_BIBR]."
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"Moreover, interferon-alpha increased the expression of interferon stimulated gene 15 (ISG15), ubiquitin specific peptidase 18 (USP18), and interleukin-6 (IL-6) via activation of STAT1."
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"In contrast, in those cells that progressed beyond this phase, the IFN treatment could not initiate USP18 induction until the next cell cycle, resulting in extended delay times proportional to the times needed to reach the next cell cycle."
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"The inductions of un phosphorylated IFN stimulated gene factor 3 (U-ISGF3) -associated ISGs, IFN stimulated gene 15 (ISG15) and ubiquitin specific protease 18 (USP18), were also evaluated."
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"Yet, the amount of ISGylated SKP2 is rather small, even in a context where global ISGylation is high as in IFN stimulated USP18 deficient fibroblasts."
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"The IFN induced Janus kinase (Jak)-signal transducer and activator of transcription protein (STAT) pathway was less frequently activated in patients with cleaved MAVS, and there was a significant inverse correlation between cleavage of MAVS and the expression level of the IFN stimulated genes IFI44L, Viperin, IFI27, USP18, and STAT1."
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"The expression of USP18 is strongly induced by type I and type III interferons [ 2-5 ] , by the Toll-like receptor ( TLR ) agonists LPS [ 6-8 ] and polyI :C [ 6 ] ( synthetic analogy of dsRNA ) and by TNFalpha [ 7 ] ."
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"A keynote presentation by Glenn Randall (University of Chicago, USA) summarized the current understanding of the mechanisms by which interferon (IFN) controls HCV infection and described how 2 key IFN stimulated genes (ISGs), ISG15 and USP18, function within a protein modification cycle to regulate hepatic innate immunity and virus infection."
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"The kinetics of USP18 upregulation by IFN is heterogeneous in single cells."
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"Firstly, like ISG15 itself, the predominant ISG15 conjugation and deconjugation enzymes UbE1L, UbcH8 and UbcM8, HERC5 and HERC6, and UBP43 and USP18 are all induced by type I IFN stimulation."
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"Usp18 is strongly upregulated by type I and type III IFNs [ 33,35,37,51,52 ] , lipopolysaccharides [ 53,54 ] , polyI :C [ 53 ] , tumor necrosis factor alpha ( TNFalpha ) [ 54 ] , or genotoxic stresses [ 35,55 ] ."
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"If cells are exposed to IFN when they pass the G1/S phases, the IFN treatment can not initiate USP18 induction until the G1 phase of the next cell cycle, causing a dramatic delay in the induction kinetics."
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"Further mutation assays revealed that the distant ISRE motif primarily contributed to the induction of zebrafish USP18 by fish IFN and IFN stimuli."
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"To further delineate the cause of the decreased chemokine production the expression of 2 essential ISGs in the IFN stimulated PBMC, USP18, and IRF7 was investigated."
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"USP18 is transcriptionally upregulated by IFN treatment and exerts inhibition of IFN-alpha signaling at the receptor level, forming a negative feedback loop."
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"Further temporal regulation of the ISG15 system by expression of the type I IFN-induced cellular deconjugase (human Usp18/mouse Ubp43), as well the role of free intracellular ISG15 in downregulating signaling at the type I IFN receptor in human cells, remains to be explored.We have shown that ISG15 is secreted from both lymphocytes and epithelial cells, suggesting that the ISG15 secretion mechanism is operational in a wide range of cell types."
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"Importantly, all three conjugation enzymes (UBA7, Ube2L6, and Herc5) as well as Usp18 are induced at the transcriptional level by Type 1 IFN signaling."
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"USP18 is transcriptionally upregulated by IFN treatment and exerts inhibition of IFN-a signaling at the receptor level, forming a negative feedback loop (Sarasin-Filipowicz et al., 2009; Franc ois-Newton et al., 2011; Arimoto et al., 2017; Malakhova et al., 2006)."
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"Another susceptibility gene in the type I interferon induced pathway is USP18."
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"b | Intracellular functions : Ubl carboxy-terminal hydrolase 18 ( USP18 ) and S-phase kinase-associated protein 2 ( SKP2 ) : USP18 , which is induced by type I interferons , mediates the negative feedback regulation of interferon signalling independent of its deISGylase activity ."
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"Since type 1 interferons (IFN) are known to induce IL10 and CD274, we next examined gene expression of the type 1 IFN induced response genes MX1 and USP18."
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"USP18 has been known to be induced by viral infection, genotoxic stress or interferon [97]."
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