Involvement of the IRF family transcription factor IRF-3 in virus-induced activation of the IFN-beta gene

FEBS Lett. 1998 Mar 20;425(1):112-6. doi: 10.1016/s0014-5793(98)00210-5.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3T3 Cells
  • Animals
  • Biological Transport
  • DNA-Binding Proteins / metabolism
  • DNA-Binding Proteins / physiology*
  • E1A-Associated p300 Protein
  • Gene Expression Regulation / physiology*
  • Interferon Regulatory Factor-3
  • Interferon-beta / genetics*
  • Mice
  • Nuclear Proteins / metabolism
  • Phosphorylation
  • Trans-Activators*
  • Transcription Factors / metabolism
  • Transcription Factors / physiology*

Substances

  • DNA-Binding Proteins
  • Interferon Regulatory Factor-3
  • Irf3 protein, mouse
  • Nuclear Proteins
  • Trans-Activators
  • Transcription Factors
  • Interferon-beta
  • E1A-Associated p300 Protein
  • Ep300 protein, mouse