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 |
卷 | 581 |
發行號 | 29 |
DOIs | |
出版狀態 | 已發佈 - 12月 11 2007 |
對外發佈 | 是 |
ASJC Scopus subject areas
- 遺傳學
- 分子生物學
- 生物物理學
- 結構生物學
- 生物化學
- 細胞生物學