IndraLab

Statements


USP18 inhibits IFN receptor. 5 / 5
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"Whereas ISG15 conjugation has been widely recognized to act antivirally 13, unconjugated ISG15 serves a proviral role by promoting USP18 mediated suppression of type I IFN receptor (IFNAR) signaling XREF_BIBR, XREF_BIBR, XREF_BIBR; this latter function of ISG15 is responsible for over-amplified ISG induction and fortified viral resistance in humans with inherited ISG15 deficiency."

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"USP18 is upregulated by type I IFNs and interacts with STAT2 to negatively regulate type I IFN receptor signaling, while ISG15 binds and stabilizes USP18."

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"On the other hand, the deubiquitinating enzyme USP18 can also directly inhibit type I IFN receptor signaling, thereby suppressing the immune response (Arimoto et al., 2017)."

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"A majority of these genes are responsible for the regulation and control of early innate inflammation, such as USP18, which disrupts the JAK-STAT pathway downstream of the IFN receptor (43), and TIFAB, which inhibits the activation of the NF-κB pathway (44)."

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"USP18 regulates antiviral responses by removing ISG15 conjugates and can directly inhibit type I IFN receptor signaling by binding the subunit 2 of the receptor via STAT-2 XREF_BIBR, XREF_BIBR."