Lopez Martin A, Meier Daniel, Wong W Wei-Lynn, Fontana Adriano
Institute of Experimental Immunology, University of Zurich, 8057 Zurich, Switzerland.
Biochem Biophys Rep. 2015 Nov 14;5:22-26. doi: 10.1016/j.bbrep.2015.11.007. eCollection 2016 Mar.
The circadian clock is required for the rhythmic expression of a plethora of genes that orchestrate metabolism, sleep-wake behaviour and the immune response to pathogens. The cold-inducible RNA binding protein (CIRBP) is required for high amplitude expression of clock genes. Moreover, CIRBP protects the expression of clock genes from the inhibitory effects of tumour necrosis factor (TNF). However, since TNF represses expression, the protective effect of CIRBP is lost. Here, we show that the TNF effect on requires the non-canonical NF-κB signalling pathway. While a knock down of RelA does not alter the effects of TNF on a knock down of RelB represses this effect. In addition, the data indicate that p50 and p52 are required in the TNF induced inhibition of . These results show that expression in TNF treated cells is regulated via the non-canonical NF-κB pathway.
昼夜节律钟对于众多协调新陈代谢、睡眠-觉醒行为以及对病原体免疫反应的基因的节律性表达是必需的。冷诱导RNA结合蛋白（CIRBP）对于生物钟基因的高振幅表达是必需的。此外，CIRBP保护生物钟基因的表达免受肿瘤坏死因子（TNF）的抑制作用。然而，由于TNF抑制表达，CIRBP的保护作用丧失。在这里，我们表明TNF对[此处原文缺失具体内容]的影响需要非经典NF-κB信号通路。虽然RelA的敲低不会改变TNF对[此处原文缺失具体内容]的影响，但RelB的敲低会抑制这种影响。此外，数据表明p50和p52在TNF诱导的对[此处原文缺失具体内容]的抑制中是必需的。这些结果表明，TNF处理细胞中的[此处原文缺失具体内容]表达是通过非经典NF-κB途径调节的。
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