Sato M, Tanaka N, Hata N, Oda E, Taniguchi T
Department of Immunology, Graduate School of Medicine and Faculty of Medicine, University of Tokyo, Japan.
FEBS Lett. 1998 Mar 20;425(1):112-6. doi: 10.1016/s0014-5793(98)00210-5.
The virus-induced activation of interferon alpha/beta (IFN-alpha/beta) gene transcription is essential for host defense. The IFN-beta promoter is controlled primarily by the virus-inducible enhancer elements, the IRF-Es. Here we show that IRF-3, an IRF family transcription factor, translocates to the nucleus from the cytoplasm upon virus infection in NIH/3T3 cells. The nuclear IRF-3 is phosphorylated, interacts with the co-activators CBP/p300, and binds specifically to the IFN-beta IRF-E. Furthermore, overexpression of IRF-3 causes a marked increase in virus-induced IFN-beta mRNA expression. Thus, IRF-3 is a candidate transcription factor mediating the activation of the IFN-beta gene.
病毒诱导的α/β干扰素(IFN-α/β)基因转录激活对于宿主防御至关重要。IFN-β启动子主要受病毒诱导的增强子元件即IRF-Es调控。在此我们表明,IRF-3(一种IRF家族转录因子)在NIH/3T3细胞被病毒感染后从细胞质转位至细胞核。细胞核内的IRF-3发生磷酸化,与共激活因子CBP/p300相互作用,并特异性结合IFN-β的IRF-E。此外,IRF-3的过表达导致病毒诱导的IFN-β mRNA表达显著增加。因此,IRF-3是介导IFN-β基因激活的候选转录因子。