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细胞因子处理后人肝癌细胞系中 NF-κB 调节的另一个长期机制。

An additional long-term mechanism of NF-κB regulation after cytokine treatment in a human hepatoma cell line.

机构信息

Institute of Anatomy and Cell Biology II, University of Heidelberg, Germany.

出版信息

Virchows Arch. 2010 Nov;457(5):585-95. doi: 10.1007/s00428-010-0970-0. Epub 2010 Sep 23.

Abstract

The eukaryotic transcription factor nuclear factor-κB (NF-κB) is mainly involved in the regulation of immune response and inflammation. A prolonged activation of NF-κB has been reported in context with chronic diseases. What leads to a prolongation of NF-κB activity is not well understood. Here, an increase in total intracellular NF-κB protein and mRNA levels as well as a temporary colocalization of NF-κB with proteasomes in human hepatocytes after treatment with TNF-α or IL-1β is reported. This indicates that beside an instantaneous activation of NF-κB and partly autoregulated inactivation by breakdown and synthesis of the inhibitors of NF-κB (IκBs), there are also mechanisms for a long-term regulation by de novo-synthesis and degradation of NF-κB protein.

摘要

真核转录因子核因子-κB(NF-κB)主要参与免疫反应和炎症的调节。据报道,NF-κB 的长期激活与慢性疾病有关。导致 NF-κB 活性延长的原因尚不清楚。本文报道了 TNF-α或 IL-1β处理人肝细胞后,细胞内总 NF-κB 蛋白和 mRNA 水平增加,以及 NF-κB 与蛋白酶体的短暂共定位。这表明,除了 NF-κB 的瞬时激活和部分由 NF-κB 抑制剂(IκBs)的降解和合成的自动失活外,NF-κB 蛋白的从头合成和降解也为长期调控提供了机制。

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