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Papers In Press, published online ahead of print November 2, 2004
Department of Molecular and Cellular Biochemistry, Kyushu University, Fukuoka, Fukuoka 812-8582
Corresponding Author: tmuta{at}mailserver.med.kyushu-u.ac.jp
We have recently identified an inducible NF-
J. Biol. Chem, 10.1074/jbc.M409983200
Submitted on August 31, 2004
Revised on November 1, 2004
Accepted on November 2, 2004
Stimulus-specific induction of a novel NF-
B regulator, IB-
, via toll/interleukin-1 receptor is mediated by mRNA stabilization
B regulator, IB-
, which is induced by microbial ligands for Toll-like receptors (TLRs) such as lipopolysaccharide (LPS) and the proinflammatory cytokine interleukin (IL)-1
, but not by tumor necrosis factor (TNF)-
. In the present study, we examined mechanisms for stimulus-specific induction of IB-. The analysis of the IB- promoter revealed an essential role for an NF-B binding sequence in transcriptional activation. The activation, however, did not account for the TLR/IL-1 receptor-specific induction of IB-, since the promoter analysis and nuclear run-on analysis indicated that its transcription was similarly induced by TNF-. To examine post-transcriptional regulation, we analyzed the decay of IB- mRNA and found that it was specifically stabilized by LPS or IL-1, but not by TNF-. Furthermore, we found that costimulation with TNF- and another proinflammatory cytokine, IL-17, elicited the IB- induction. Stimulation with IL-17 alone did not induce IB- but stabilized its mRNA. Therefore, IB- induction requires both NF-B activation and stimulus-specific stabilization of its mRNA. Since IB- is essential for expression of a subset of NF-B target genes, the stimulus-specific induction of IB- may be of great significance in regulation of inflammatory reactions.
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