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© Research
Publication : Nature structural & molecular biology

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

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Nature structural & molecular biology - 06 Feb 2017

Arimoto KI, Löchte S, Stoner SA, Burkart C, Zhang Y, Miyauchi S, Wilmes S, Fan JB, Heinisch JJ, Li Z, Yan M, Pellegrini S, Colland F, Piehler J, Zhang DE

Link to Pubmed [PMID] – 28165510

Nat. Struct. Mol. Biol. 2017 Mar;24(3):279-289

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.

https://www.ncbi.nlm.nih.gov/pubmed/28165510