首页> 美国卫生研究院文献>Inflammatory Bowel Diseases >Ablation of Gly96/Immediate Early Gene-X1 (gly96/iex-1) Aggravates DSS-Induced Colitis in Mice: Role for gly96/iex-1 in the Regulation of NF-κB
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Ablation of Gly96/Immediate Early Gene-X1 (gly96/iex-1) Aggravates DSS-Induced Colitis in Mice: Role for gly96/iex-1 in the Regulation of NF-κB

机译:Gly96 /立即早期基因X1(gly96 / iex-1)的消融加重了DSS诱导的小鼠结肠炎:gly96 / iex-1在调节NF-κB中的作用

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摘要

BackgroundInflammatory bowel diseases (IBDs) result from environmental and genetic factors and are characterized by an imbalanced immune response in the gut and deregulated activation of the transcription factor NF-κB. Addressing the potential role of gly96/iex-1 in the regulation of NF-κB in IBD, we used the dextran sodium sulfate (DSS) colitis model in mice in which the gly96/iex-1 gene had been deleted.
机译:背景炎症性肠病(IBD)由环境和遗传因素导致,其特征是肠道免疫反应失衡以及转录因子NF-κB的激活失控。为了解决IBD中gly96 / iex-1在调节NF-κB中的潜在作用,我们在已删除了gly96 / iex-1基因的小鼠中使用了葡聚糖硫酸钠(DSS)结肠炎模型。

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