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STAT2 is an essential adaptor in USP18-mediated suppression of type I interferon signaling.

Abstract : 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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https://hal-pasteur.archives-ouvertes.fr/pasteur-02071003
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Submitted on : Monday, March 18, 2019 - 12:51:33 PM
Last modification on : Monday, January 13, 2020 - 5:08:09 PM

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Kei-Ichiro Arimoto, Sara Löchte, Samuel Stoner, Christoph Burkart, Yue Zhang, et al.. STAT2 is an essential adaptor in USP18-mediated suppression of type I interferon signaling.. Nature Structural and Molecular Biology, Nature Publishing Group, 2017, 24 (3), pp.279-289. ⟨10.1038/nsmb.3378⟩. ⟨pasteur-02071003⟩

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