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首页> 外文期刊>Biochemical Pharmacology >P23 co-chaperone protects the aryl hydrocarbon receptor from degradation in mouse and human cell lines
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P23 co-chaperone protects the aryl hydrocarbon receptor from degradation in mouse and human cell lines

机译：P23伴侣伴侣保护芳烃受体免受小鼠和人类细胞系降解

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摘要

The aryl hydrocarbon receptor (AhR) is a ligand-sensitive transcription factor which is responsible for most 2,3,7,8-tetrachlorodibenzo-p-dioxin toxicities. Without ligand, the AhR complex is cytoplasmic and contains p23. Our objective was to investigate whether the wild type p23 levels are important for the AhR function. We generated eight p23-specific knockdown stable cell lines via either electroporation or lentiviral infection. Five of these stable cell lines were generated from a mouse hepatoma cell line (Hepa1c1c7) and three were from human hepatoma and cervical cell lines (Hep3B and HeLa). All of them expressed lower AhR protein levels, leading to reduced ligand-induced, DRE-driven downstream activity. The AhR protein levels in p23-specific knockdown stable cells were reversed back to wild type levels after exogenous p23 was introduced. Reduction of the AhR protein levels in these stable cells was caused by a decrease in the AhR message levels and an increase of the AhR protein degradation in the absence of ligand. This ligand-independent degradation of AhR was not reversed by MG132, suggesting that the 26S proteasome was not responsible for the degradation. In addition, MG132 could not protect AhR from the ligand-induced degradation in both mouse and human p23-knockdown stable cells.
机译：芳基烃受体（AhR）是一种配体敏感的转录因子，可引起大多数2,3,7,8-四氯二苯并-p-二恶英毒性。没有配体，AhR复合物是胞质的，含有p23。我们的目标是研究野生型p23水平对AhR功能是否重要。我们通过电穿孔或慢病毒感染产生了八个p23特异性的基因敲除稳定细胞系。这些稳定的细胞系中有五个是从小鼠肝癌细胞系（Hepa1c1c7）产生的，另外三个是从人肝癌和宫颈细胞系（Hep3B和HeLa）产生的。它们都表达较低的AhR蛋白水平，从而导致配体诱导的DRE驱动的下游活性降低。引入外源性p23后，p23特异性敲低稳定细胞中的AhR蛋白水平被逆转回野生型水平。这些稳定细胞中AhR蛋白水平的降低是由于在没有配体的情况下AhR信息水平的降低和AhR蛋白降解的增加所致。 MG132并未逆转这种非配体依赖性的AhR降解，表明26S蛋白酶体对降解不负责。此外，MG132不能保护AhR免受配体诱导的小鼠和人类p23基因敲低稳定细胞的降解。

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