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首页> 外文期刊>Cell metabolism >BRD7 regulates XBP1s' activity and glucose homeostasis through its interaction with the regulatory subunits of PI3K
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BRD7 regulates XBP1s' activity and glucose homeostasis through its interaction with the regulatory subunits of PI3K

机译：BRD7通过与PI3K的调节亚基相互作用来调节XBP1的活性和葡萄糖稳态。

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摘要

Bromodomain-containing protein 7 (BRD7) is a member of the bromodomain-containing protein family that is known to play a role as tumor suppressors. Here, we show that BRD7 is a component of the unfolded protein response (UPR) signaling through its ability to regulate X-box binding protein 1 (XBP1) nuclear translocation. BRD7 interacts with the regulatory subunits of phosphatidylinositol 3-kinase (PI3K) and increases the nuclear translocation of both p85α and p85β and the spliced form of XBP1 (XBP1s). Deficiency of BRD7 blocks the nuclear translocation of XBP1s. Furthermore, our in vivo studies have shown that BRD7 protein levels are reduced in the liver of obese mice, and reinstating BRD7 levels in the liver restores XBP1s nuclear translocation, improves glucose homeostasis, and ultimately reduces the blood glucose levels in the obese and diabetic mouse models.
机译：含溴结构域的蛋白质7（BRD7）是含溴结构域的蛋白质家族的成员，已知该家族起着抑癌作用。在这里，我们显示BRD7是通过其调节X-box结合蛋白1（XBP1）核易位的能力而成为未折叠蛋白应答（UPR）信号的组成部分。 BRD7与磷脂酰肌醇3-激酶（PI3K）的调节亚基相互作用，并增加p85α和p85β的核易位以及XBP1（XBP1s）的剪接形式。 BRD7的缺乏会阻碍XBP1的核易位。此外，我们的体内研究表明，肥胖小鼠肝脏中的BRD7蛋白水平降低，并且肝脏中BRD7水平的恢复可恢复XBP1s的核易位，改善葡萄糖稳态，并最终降低肥胖和糖尿病小鼠的血糖水平楷模。

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