IndraLab

Statements

USP18 inhibits JAK-STAT. 11 / 11
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"USP18 was shown to bind to IFNAR2 and attenuate the JAK-STAT pathway, thereby negatively regulating IFN signaling (XREF_TABLE)."
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"However, it has been shown that USP18 negatively regulates the JAK-STAT pathway, and more generally cellular responses to type I IFN, independently of its ISG15 isopeptidase activity [85] ."
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"USP18, which is known to negatively regulates the JAK-STAT pathway, and, as such, is a broad-spectrum pro-viral factor, 39 was identified during our screen as a pro-ZIKV candidate in HMC3 cells ( Figu[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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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, and TIFAB which inhibits the activation of the NFkappaB pathway."
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"Recent data by Zhang and coworkers revealed, however, that USP18 attenuates JAK-STAT signaling, and thereby the type 1 IFN response, in a non enzymatic manner, i.e., by directly competing with JAK1 for binding to the IFNAR2 subunit of the type 1 IFN receptor."
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"In contrast, binding this free ISG15, USP18 suppresses JAK-STAT signaling further counteracting IFN signaling.By better understanding the ISG15 pathway, it may be possible to target certain illnesses on a case-by-case basis without the need for general activation of IFN signaling with its hundreds of downstream targets."
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"We found that, beyond being a key effector of IFN signaling, STAT2 is essential for USP18 mediated inhibition of JAK-STAT signaling."
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"Recent data by Zhang and coworkers ( Malakhova et al ., 2006 ) revealed , however , that USP18 attenuates JAK-STAT signaling , and thereby the type 1 IFN response , in a non-enzymatic manner , i.e ., by directly competing with JAK1 for binding to the IFNAR2 subunit of the type 1 IFN receptor ."
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"For instance, USP18, a negative regulator of IFN response, inhibits JAK-STAT signaling pathway (45)."
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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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"Another ISG : the ubiquitin-specific peptidase 18 ( USP18 ) suppresses JAK-STAT signaling induced by type I IFN at the level of IFN receptor ."
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