IndraLab

Statements

USP18 inhibits IFN-I. 11 / 11
| 11
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"We show that the hyper-active IFN-I signaling cascade causes increased induction of the IFNAR negative regulator USP18, in turn hyper-suppressing any subsequent response to IFN-I and effectively repressing further antiviral responses."
36243008
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"Therefore, under the circumstances of enhanced IFN-I signaling caused by USP18 deletion, IFN-I-inducible E2 enzyme UBCH5 likely enhances the activity of E3 ligase NEDD4, leading to degradation of CSF1R via the ubiquitin-proteasome system.Since NEDD4 is frequently overexpressed in cancers, including prostate, bladder, and colon cancers, NEDD4 was originally thought to be an oncogene."
38100351
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"The mechanism by which MARCH1 regulates IFN-I remains obscure and several factors may include increased expression of genes encoding SOCS1, SOCS3, SIKE1, CACTIN, TRIM24, IL-10RA, USP18, and mir-21 that are known to suppress IFN-I responses and changes in DCs, Macs, and other cell populations can may also affect the levels of proteins critical for IFN-I production."
33363057
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"In mice, Usp18 negatively regulates Stat1 activation and the downstream IFN-I response by interaction with Ifnar2, and mice lacking Usp18 in microglia display brain disease due to uncontrolled IFN-I signalling [6]."
36753016
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"During systemic infection with the vesicular stomatitis virus (VSV), CD169 + macrophages of the splenic marginal zone and the lymph node sinusoid can express the endogenous IFN-I blocker Usp18, thereby promoting virus replication and enhancing the antiviral immune response [XREF_BIBR, XREF_BIBR]."
| PMC
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"Deletion of USP18 enhances and prolongs IFN-I signaling and expands the pool of IFN-inducible genes."
38100351
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"Given that Usp18 inhibits IFN-I signaling, it will be important to further understand why increases in Usp18 expression do not correlate with a corresponding decrease in IFN-I stimulated gene expression."
26783074
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"The mechanism by which USP18 inhibits the IFN-I response to promote cancer progression has been elucidated in detail (14)."
38596661
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"Following exposure to IFN-I, metallophilic macrophages induce expression of the Usp18 protein which prevents Jak1 phosphorylation and inhibits IFN-I signaling in these cells."
27769506
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"Therefore enhanced activity of Usp18 in beta islet cells would limit IFN-I signaling in these cells and could prevent diabetes during exposure to IFN-I XREF_BIBR."
24204252
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"Enhanced IFN-I signaling and blocked USP18 expression prompt downregulation of colony stimulating factor 1 receptor (CSF1R) and polarization of tumor-associated macrophages toward pro-inflammatory phenotypes."
38100351