Osmotic stress blocks NF-κB-dependent inflammatory responses by inhibiting ubiquitination of IκB

Wei Chun HuangFu, Kunihiro Matsumoto, Jun Ninomiya-Tsuji

研究成果: 雜誌貢獻文章同行評審

3 引文 斯高帕斯(Scopus)

摘要

The inhibitory effects of hypertonic conditions on immune responses have been described in clinical studies; however, the molecular mechanism underlying this phenomenon has yet to be defined. Here we investigate osmotic stress-mediated modification of the NF-κB pathway, a central signaling pathway in inflammation. We unexpectedly found that osmotic stress could activate IκBα kinase but did not activate NF-κB. Osmotic stress-induced phosphorylated IκBα was not ubiquitinated, and osmotic stress inhibited interleukin 1-induced ubiquitination of IκBα and ultimately blocked expression of cytokine/chemokines. Thus, blockage of IκBα ubiquitination is likely to be a major mechanism for inhibition of inflammation by hypertonic conditions.
原文英語
頁(從 - 到)5549-5554
頁數6
期刊FEBS Letters
581
發行號29
DOIs
出版狀態已發佈 - 12月 11 2007
對外發佈

ASJC Scopus subject areas

  • 生物化學
  • 生物物理學
  • 分子生物學

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