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首页> 外文期刊>The FEBS journal >Nuclear factor-erythroid 2-related factor 1 regulates expression of proteasome genes in hepatocytes and protects against endoplasmic reticulum stress and steatosis in mice.
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Nuclear factor-erythroid 2-related factor 1 regulates expression of proteasome genes in hepatocytes and protects against endoplasmic reticulum stress and steatosis in mice.

机译：核因子-类胡萝卜素2相关因子1调节小鼠肝细胞中蛋白酶体基因的表达，并防止内质网应激和脂肪变性。

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The ubiquitin-proteasome system is important in maintaining protein homeostasis. NFE2-related factor 1 (Nrf1), a transcription factor in the cap 'n' collar basic-leucine zipper family, regulates expression of cytoprotective genes. It was previously shown that liver-specific knockout of Nrf1 (Nrf1LKO) leads to hepatic cell death, steatohepatitis and cancer. However, the mechanisms underlying these pathologies are not clear. Here, we report that Nrf1 is critical for proteasome gene expression in the liver. Liver-specific knockout of Nrf1 results in impaired basal and induced expression of proteasome genes, and diminished proteasome activity in hepatocytes. In addition, our findings demonstrated that endoplasmic reticulum stress signaling pathway was also activated in Nrf1LKO livers. Inhibition of proteasome activity leads to endoplasmic reticulum stress in Nrf1-deficient hepatocytes, prompting the development of steatosis in the liver. Our results indicate that Nrf1 plays an integral role in the maintenance of proteasome function in hepatocytes and in the prevention of liver steatosis development. Moreover, these results highlight an association between proteasome dysfunction, endoplasmic reticulum stress and steatosis. 2013. This article is a U.S. Government work and is in the public domain in the USA.Registry Number/Name of Substance 0 (Boronic Acids). 0 (NF-E2-Related Factor 1). 0 (Nfe2L1 protein, mouse). 0 (Pyrazines). 0 (bortezomib). EC 3-4-25-1 (Proteasome Endopeptidase Complex).
机译：泛素-蛋白酶体系统在维持蛋白质稳态方面很重要。 NFE2相关因子1（Nrf1）是cap'n'衣领碱性亮氨酸拉链家族中的转录因子，调节细胞保护性基因的表达。先前显示，肝脏特异性的Nrf1（Nrf1LKO）敲除会导致肝细胞死亡，脂肪性肝炎和癌症。但是，这些病理的潜在机制尚不清楚。在这里，我们报道Nrf1对肝脏中的蛋白酶体基因表达至关重要。 Nrf1的肝脏特异性敲除导致蛋白酶体基因的基础和诱导表达受损，并降低了肝细胞中的蛋白酶体活性。此外，我们的研究结果表明，Nrf1LKO肝内质网应激信号通路也被激活。蛋白酶体活性的抑制导致缺乏Nrf1的肝细胞内质网应激，促使肝脏脂肪变性的发展。我们的结果表明，Nrf1在维持肝细胞蛋白酶体功能和预防肝脂肪变性中起着不可或缺的作用。而且，这些结果突出了蛋白酶体功能障碍，内质网应激和脂肪变性之间的关联。 2013。本文是美国政府的工作，在美国属于公共领域。注册号/物质0（硼酸）的名称。 0（NF-E2相关因子1）。 0（Nfe2L1蛋白，小鼠）。 0（吡嗪）。 0（硼替佐米）。 EC 3-4-25-1（蛋白酶体内肽酶复合物）。

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