c-Cbl诱导的多多素泛化有助于在糖尿病病中损伤细胞
Lulu Liang1,2,3,4, Mengfei He1,2,3,4, Panpan Zhou1,2,3,4
1Department of Nephrology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
概括
糖尿病病 (DN) 涉及脏中蛋白质无化变化的情况. 波多辛的泛基化,特别是在K261R,有助于波多细胞损伤和蛋白尿,其中c-Cbl起着关键作用.
科学领域:
- 腎臟病學 (nephrology) 是一種醫學專業.
- 分子生物学分子生物学
- 蛋白质组学是指蛋白质组学.
背景情况:
- 糖尿病病 (DN) 是糖尿病的一个主要并发症,其特点是损伤和蛋白尿.
- 蛋白质无处不在在DN病原发生中的作用越来越被认可,但缺乏全面的无处不在性特征.
- 了解DN中的无处不在变化对于确定治疗点至关重要.
研究的目的:
- 为了研究糖尿病 (db/db) 鼠与非糖尿病 (db/m) 对照鼠的脏中蛋白质泛化概况的差异.
- 为了识别特定的无处不在的蛋白质和DN中改变的位点.
- 探索多多素无处不在的作用及其在DN中的调节因素.
主要方法:
- 液体染色学-质谱学 (LC-MS/MS) 用于分析脏的无处不在物质.
- 定量蛋白质组学确定了差异性无处不在的蛋白质和位点.
- 进行了亚细胞局部化和丰富性分析.
- 变异性研究和蛋白质与蛋白质相互作用试验被用来调查多多 ubiquitination.
主要成果:
- 在db/db小鼠脏中观察到泛化显著变化,发现了许多高调和低调的泛化蛋白和部位.
- 在与紧密结合,氧化酸化和热生成相关的途径中,化蛋白质得到了丰富.
- 在DN条件下,Podocin是一种关键的切割膜膜蛋白,在K261R部位显示出降低的泛化.
- 发现E3酶c-Cbl可以结合多多并影响其无处不在.
结论:
- 蛋白质泛化,特别是K261R中的多多辛,在糖尿病病中显著改变,并导致多多细胞损伤.
- c-Cbl参与调节皮多辛无化,并代表一个潜在的治疗点,以保持皮多细胞完整性和减少DNA中的蛋白尿症.
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