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. 2017 Nov 18;8(62):105923–105935. doi: 10.18632/oncotarget.22510

Figure 8. A hypothetical model of IRS4/USP18 interaction and its role in IFN antiviral function.

Figure 8

USP18 binding to IFNAR2 in vivo blocks the interaction between Jak and the IFN receptor, thereby reduces the phosphorylation of the receptor and STATs and suppresses signal pathway. The interaction between IRS4 and USP18 decreased the inhibitory effect of USP18 on Jak/STAT signaling pathway. Therefore, IRS4 enhanced IFN-α induced activation of the Jak/STAT signaling pathway as shown by the increased levels of p-STAT1 and enhanced ISRE activity and increased induction of ISGs.