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Distinct and essential roles of transcription factors IRF-3 and IRF-7 in response to viruses for IFN-alpha/beta gene induction.

Induction of the interferon (IFN)-alpha/beta gene transcription in virus-infected cells is an event central to innate immunity. Mice lacking the transcription factor IRF-3 are more vulnerable to virus infection. In embryonic fibroblasts, virus-induced IFN-alpha/beta gene expression levels are reduced and the spectrum of the IFN-alpha mRNA subspecies altered. Furthermore, cells additionally defective in IRF-7 expression totally fail to induce these genes in response to infections by any of the virus types tested. In these cells, a normal profile of IFN-alpha/beta mRNA induction can be achieved by coexpressing both IRF-3 and IRF-7. These results demonstrate the essential and distinct roles of thetwo factors, which together ensure the transcriptional efficiency and diversity of IFN-alpha/beta genes for the antiviral response.

Pubmed ID: 11070172

Authors

  • Sato M
  • Suemori H
  • Hata N
  • Asagiri M
  • Ogasawara K
  • Nakao K
  • Nakaya T
  • Katsuki M
  • Noguchi S
  • Tanaka N
  • Taniguchi T

Journal

Immunity

Publication Data

October 8, 2000

Associated Grants

None

Mesh Terms

  • Animals
  • DNA-Binding Proteins
  • Down-Regulation
  • Embryo, Mammalian
  • Female
  • Fibroblasts
  • Gene Expression Regulation
  • Gene Targeting
  • Interferon Regulatory Factor-3
  • Interferon Regulatory Factor-7
  • Interferon Type I
  • Interferon-beta
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Mice, Transgenic
  • Newcastle disease virus
  • Promoter Regions, Genetic
  • RNA, Messenger
  • Retroviridae
  • Signal Transduction
  • Transcription Factors
  • Transcriptional Activation