作者: Akiko Eto , Tatsushi Muta , Soh Yamazaki , Koichiro Takeshige
DOI: 10.1016/S0006-291X(02)03082-6
关键词: Toll-like receptor 、 IκB kinase 、 NF-κB 、 Signal transduction 、 Tumor necrosis factor alpha 、 Receptor 、 Cell biology 、 Stimulation 、 Chemistry 、 TRAF2 、 Molecular biology
摘要: Abstract IκB-ζ, a new negative-regulator of nuclear factor-κB (NF-κB), is strongly induced by lipopolysaccharide or interleukin-1β stimulation, but not tumor necrosis factor-α. Here, we analyzed the mechanisms for transcriptional induction IκB-ζ. IκB-ζ mRNA was overexpression MyD88 TRAF6, TRAF2. Stimulation macrophages with peptidoglycan CpG DNA, which activated Toll-like receptor 2 9, respectively, also resulted in induction. Thus, activation MyD88-dependent signaling pathway, commonly found downstream different Toll/interleukin-1 (TIR) domains, sufficient The inhibited treatment various inhibitors NF-κB overexpressing IκB-α β, indicating essential roles However, subunits IκB-α, These results indicate existence another signal induction, specifically mediated TIR domain-mediated pathway.