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首页> 外文期刊>Genes to cells : >NF-kappaB signaling pathway is inhibited by heat shock independently of active transcription factor HSF1 and increased levels of inducible heat shock proteins.
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NF-kappaB signaling pathway is inhibited by heat shock independently of active transcription factor HSF1 and increased levels of inducible heat shock proteins.

机译：NF-κB信号传导途径受热激抑制而不受活性转录因子HSF1的影响，并且诱导型热激蛋白水平升高。

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摘要

NF-kappaB transcription factor regulates numerous genes important for inflammation, immune responses and cell survival. HSF1 is the primary transcription factor activated under stress conditions that is responsible for induction of genes encoding heat shock proteins. Previous studies have shown that the NF-kappaB activation pathway is blocked by heat shock possibly involving heat shock proteins. Here, we investigate whether active HSF1 inhibited this pathway in the absence of stress conditions. Activation of the NF-kappaB pathway and expression of NF-kappaB-dependent genes were analyzed in TNFalpha-stimulated U-2 OS human osteosarcoma cells that were either heat-shocked or engineered to express a constitutively active form of HSF1 in the absence of heat shock. As expected, heat shock resulted in a general blockade in the degradation of the IkappaBalpha inhibitor, nuclear translocation of NF-kappaB and expression of NF-kappaB-dependent target genes. In marked contrast, the presence of constitutively active HSF1 did not block TNFalpha-induced activation of the NF-kappaB pathway or expression of a set of the NF-kappaB-dependent genes. We conclude that in the absence of heat shock, the NF-kappaB activation pathway is inhibited by neither active HSF1 transcription factor nor by increased levels of HSF1-induced heat shock proteins. Copyright 2011 The Authors. Journal compilation Copyright 2011 by the Molecular Biology Society of Japan/Blackwell Publishing Ltd.
机译：NF-κB转录因子调节对炎症，免疫反应和细胞存活重要的许多基因。 HSF1是在压力条件下激活的主要转录因子，负责诱导编码热激蛋白的基因。先前的研究表明，NF-kappaB的激活途径可能受到热激蛋白的干扰而被热激蛋白阻断。在这里，我们调查了在缺乏压力条件下活性HSF1是否抑制了该途径。在TNFα刺激的U-2 OS人骨肉瘤细胞中分析了NF-kappaB途径的激活和NF-kappaB依赖性基因的表达，这些细胞被热激或经工程改造以在不存在热的情况下表达HSF1的组成型活性形式休克。不出所料，热休克导致IkappaBalpha抑制剂的降解，NF-kappaB的核易位和NF-kappaB依赖性靶基因的表达普遍受到阻滞。与之形成鲜明对比的是，组成性活性HSF1的存在并未阻断TNFα诱导的NF-κB途径的激活或一组NF-κB依赖性基因的表达。我们得出的结论是，在没有热休克的情况下，NF-κB激活途径既不受活性HSF1转录因子的抑制，也不受HSF1诱导的热休克蛋白水平升高的抑制。版权所有2011作者。期刊编辑日本分子生物学会/ Blackwell Publishing Ltd.版权所有2011。

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