由化物诱导的氧化应激参与了YTHDF2相分离过程
Jin Man1, Qian Zhang1, Tianhe Zhao1
1Department of Environmental and Occupational Health, West China School of Public Health, Sichuan University, Chengdu, 610041, Sichuan, China.
Biological trace element research
|June 13, 2023
概括
暴露于酸盐会诱导氧化应激,促进YTHDF2相分离并改变N-甲基氨酸 (m6A) 水平. 抗氧化剂N-乙半氨酸逆转了这些影响,突出了氧化应激.
科学领域:
- 分子生物学分子生物学
- 细胞生物学 细胞生物学
- 毒理学 毒理学 毒理学
背景情况:
- 在酸盐刺激时观察到YTH N6-甲基氨酸RNA结合蛋白2 (YTHDF2) 的相分离.
- 氧化应激是矿毒性的主要机制.
- 在YTHDF2相分离中,化物诱导的氧化应激作用需要阐明.
研究的目的:
- 为了研究化物诱导的氧化应激对YTHDF2相分离的影响.
- 为了确定N-甲基氨酸 (m6A) 修饰在这个过程中的参与.
主要方法:
- 人类角质细胞暴露于不同度的酸和抗氧化剂N-乙半氨酸.
- 测量了氧化应激水平,YTHDF2相分离和m6A修饰.
- 分析了m6A甲基雌激酶和脱甲基酶水平的变化.
主要成果:
- 化物暴露增加了氧化应激和YTHDF2相分离以剂量依赖的方式.
- N-乙半氨酸预处理减弱了酸盐诱导的氧化应激,并抑制了YTHDF2相分离.
- 化物暴露导致m6A水平升高,m6A甲基化酶上调和m6A脱甲基酶下调,N-乙半氨酸的作用逆转.
结论:
- 石诱导的氧化应激是YTHDF2相分离的关键驱动因素.
- 亚化物诱导的YTHDF2相分离是由m6A修饰介导的.
- 这项研究从相分离的角度提供了对石毒性机制的新见解.
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