Journal article

IFNβ-dependent increases in STAT1, STAT2, and IRF9 mediate resistance to viruses and DNA damage.

HyeonJoo Cheon, Elise G Holvey-Bates, John W Schoggins, Samuel Forster, Paul Hertzog, Naoko Imanaka, Charles M Rice, Mark W Jackson, Damian J Junk, George R Stark

The EMBO Journal | Published : 2013

Abstract

A single high dose of interferon-β (IFNβ) activates powerful cellular responses, in which many anti-viral, pro-apoptotic, and anti-proliferative proteins are highly expressed. Since some of these proteins are deleterious, cells downregulate this initial response rapidly. However, the expression of many anti-viral proteins that do no harm is sustained, prolonging a substantial part of the initial anti-viral response for days and also providing resistance to DNA damage. While the transcription factor ISGF3 (IRF9 and tyrosine-phosphorylated STATs 1 and 2) drives the first rapid response phase, the related factor un-phosphorylated ISGF3 (U-ISGF3), formed by IFNβ-induced high levels of IRF9 and S..

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University of Melbourne Researchers