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Microarray analysis of tumor necrosis factor α induced gene expression in U373 human glioblastoma cells

机译:肿瘤坏死因子α诱导的U373人胶质母细胞瘤细胞基因表达的微阵列分析

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摘要

BackgroundTumor necrosis factor α (TNF) is able to induce a variety of biological responses in the nervous system including inflammation and neuroprotection. Human astrocytoma cells U373 have been widely used as a model for inflammatory cytokine actions in the nervous system. Here we used cDNA microarrays to analyze the time course of the transcriptional response from 1 h up to 12 h post TNF treatment in comparison to untreated U373 cells. TNF activated strongly the NF-κB transcriptional pathway and is linked to other pathways via the NF-κB target genes JUNB and IRF-1. Part of the TNF-induced gene expression could be inhibited by pharmacological inhibition of NF-κB with pyrrolidine-dithiocarbamate (PDTC). NF-κB comprises a family of transcription factors which are involved in the inducible expression of genes regulating neuronal survival, inflammatory response, cancer and innate immunity.
机译:背景肿瘤坏死因子α(TNF)能够在神经系统中诱导多种生物学反应,包括炎症和神经保护。人类星形细胞瘤细胞U373已被广泛用作神经系统中炎性细胞因子作用的模型。在这里,我们使用cDNA微阵列分析了与未处理的U373细胞相比,从TNF处理后1小时到12小时的转录反应的时间过程。 TNF强烈激活NF-κB转录途径,并通过NF-κB靶基因JUNB和IRF-1与其他途径相连。吡咯烷二硫代氨基甲酸酯(PDTC)可通过药理抑制NF-κB来抑制TNF诱导的部分基因表达。 NF-κB包括一个转录因子家族,参与调节神经元存活,炎症反应,癌症和先天免疫的基因的诱导表达。

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