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Arimoto, Kei-Ichiro; Löchte, Sara; Stoner, Samuel A; Burkart, Christoph; Zhang, Yue; Miyauchi, Sayuri; Wilmes, Stephan; Fan, Jun-Bao; Heinisch, Jürgen J; Li, Zhi; Yan, Ming; Pellegrini, Sandra; Colland, Frédéric; Piehler, Jacob; Zhang, Dong-Er
Nature structural & molecular biology, 03/2017, Letnik: 24, Številka: 3Journal Article
Type I interferons (IFNs) are multifunctional cytokines that regulate immune responses and cellular functions but also can have detrimental effects on human health. A tight regulatory network therefore controls IFN signaling, which in turn may interfere with medical interventions. The JAK-STAT signaling pathway transmits the IFN extracellular signal to the nucleus, thus resulting in alterations in gene expression. STAT2 is a well-known essential and specific positive effector of type I IFN signaling. Here, we report that STAT2 is also a previously unrecognized, crucial component of the USP18-mediated negative-feedback control in both human and mouse cells. We found that STAT2 recruits USP18 to the type I IFN receptor subunit IFNAR2 via its constitutive membrane-distal STAT2-binding site. This mechanistic coupling of effector and negative-feedback functions of STAT2 may provide novel strategies for treatment of IFN-signaling-related human diseases.
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