卡帕
糖皮质激素受体
糖皮质激素
NFKB1型
免疫系统
转录因子
生物
肿瘤坏死因子α
NF-κB
化学
癌症研究
分子生物学
信号转导
免疫学
细胞生物学
基因
生物化学
哲学
语言学
作者
Robert I. Scheinman,Patricia C. Cogswell,A K Lofquist,Albert S. Baldwin
出处
期刊:Science
[American Association for the Advancement of Science (AAAS)]
日期:1995-10-13
卷期号:270 (5234): 283-286
被引量:1663
标识
DOI:10.1126/science.270.5234.283
摘要
Glucocorticoids are potent immunosuppressive drugs, but their mechanism is poorly understood. Nuclear factor kappa B (NF-kappa B), a regulator of immune system and inflammation genes, may be a target for glucocorticoid-mediated immunosuppression. The activation of NF-kappa B involves the targeted degradation of its cytoplasmic inhibitor, I kappa B alpha, and the translocation of NF-kappa B to the nucleus. Here it is shown that the synthetic glucocorticoid dexamethasone induces the transcription of the I kappa B alpha gene, which results in an increased rate of I kappa B alpha protein synthesis. Stimulation by tumor necrosis factor causes the release of NF-kappa B from I kappa B alpha. However, in the presence of dexamethasone this newly released NF-kappa B quickly reassociates with newly synthesized I kappa B alpha, thus markedly reducing the amount of NF-kappa B that translocates to the nucleus. This decrease in nuclear NF-kappa B is predicted to markedly decrease cytokine secretion and thus effectively block the activation of the immune system.
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