Roles of unphosphorylated ISGF3 in HCV infection and interferon responsiveness.
Taejŏn, South Korea. In Proc Natl Acad Sci U S A, 27 Aug 2015
Here, we investigated the mechanism of prolonged ISG expression and its role in IFN responsiveness during HCV infection in relation to unphosphorylated IFN-stimulated gene factor 3 (U-ISGF3), recently identified as a tripartite transcription factor formed by high levels of IFN response factor 9 (IRF9), STAT1, and STAT2 without tyrosine phosphorylation of the STATs.
STAT2 signaling and dengue virus infection.
Seattle, United States. In Jakstat, 2014
This review describes strategies that DENV uses to evade the type I interferon response and focuses on how data gained from the study of DENV NS5-mediated STAT2 degradation may be used to create immunocompetent DENV mouse models and design anti-DENV therapeutics.
STAT2 and IRF9: Beyond ISGF3.
Montréal, Canada. In Jakstat, 2013
Among STATs, STAT2 is classically known to dimerize with STAT1 and together with IRF9 forms the ISGF3 transcription factor complex that has long been considered a hallmark of activation by type I and type III interferons.
STATs get their move on.
Stony Brook, United States. In Jakstat, 2013
Following STAT2 tyrosine phosphorylation, it can form dimers with STAT1 to affect nuclear import as the trimeric complex (ISGF3).
The JAK-STAT pathway at twenty.
Cleveland, United States. In Immunity, 2012
We look back on the discoveries that the tyrosine kinases TYK2 and JAK1 and the transcription factors STAT1, STAT2, and IRF9 are required for the cellular response to type I interferons.