Abstract
Stimulus-specific Induction of a Novel Nuclear Factor-κB Regulator, IκB-ζ, via Toll/Interleukin-1 Receptor Is Mediated by mRNA Stabilization
Highlights
Cells reprogram gene expression upon environmental changes to maintain homeostasis
We have recently identified an inducible nuclear factor-B (NF-B) regulator, IB-, which is induced by microbial ligands for Toll-like receptors such as lipopolysaccharide and the proinflammatory cytokine interleukin (IL)-1 but not by tumor necrosis factor (TNF)-␣
IB- Is Induced by Stimulation of toll-like receptors (TLRs)/IL-1 receptor (IL-1R)— Our previous studies have demonstrated the essential requirement of an unidentified signal(s) for IB- induction that comes from the TIR domain, in addition to Nuclear factor-B (NF-B) activation [18]
Summary
Cells reprogram gene expression upon environmental changes to maintain homeostasis. For multicellular organisms, serious environmental changes include microbial infection, and a major rearrangement of gene expression occurs during inflammatory responses against infection. We found that stability of IB- mRNA was up-regulated by stimulation with LPS or IL-1 but not with TNF-␣. This finding indicates that in addition to NF-B activation, the other signal required for IB- induction, which comes from the TIR domain but not from the TNF-␣ receptor, leads to mRNA stabilization.
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