Essential roles for NF-κB and a Toll/IL-1 receptor domain-specific signal(s) in the induction of IκB-ζ

Akiko Eto, Tatsushi Muta, Soh Yamazaki, Koichiro Takeshige

Research output: Contribution to journalArticle

43 Citations (Scopus)

Abstract

IκB-ζ, a new negative-regulator of nuclear factor-κB (NF-κB), is strongly induced by lipopolysaccharide or interleukin-1β stimulation, but not by tumor necrosis factor-α. Here, we analyzed the mechanisms for transcriptional induction of IκB-ζ. IκB-ζ mRNA was induced by overexpression of MyD88 or TRAF6, but not TRAF2. Stimulation of macrophages with peptidoglycan or CpG DNA, which activated Toll-like receptor 2 or 9, respectively, also resulted in IκB-ζ induction. Thus, activation of the MyD88-dependent signaling pathway, commonly found downstream of different Toll/interleukin-1 receptor (TIR) domains, is sufficient for IκB-ζ induction. The induction was inhibited by treatment with various inhibitors of NF-κB activation or by overexpressing IκB-α or β, indicating essential roles for NF-κB in IκB-ζ induction. However, overexpression of the NF-κB subunits induced IκB-α, but not IκB-ζ. These results indicate the existence of another signal essential for IκB-ζ induction, which is specifically mediated by the TIR domain-mediated signaling pathway.

Original languageEnglish
Pages (from-to)495-501
Number of pages7
JournalBiochemical and biophysical research communications
Volume301
Issue number2
DOIs
Publication statusPublished - 2003 Feb 7

Keywords

  • Innate immunity
  • IκB-ζ
  • Macrophage
  • Nuclear factor-κB
  • Toll-like receptor
  • Toll/interleukin-1 receptor domain
  • Transcriptional induction

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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