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m6A阅读器IGF2BP1通过识别m6A修饰来减弱RPL36的稳定性和细胞增殖,以调节甲酸血毒性

Jingyu Wang¹, Xiaoli Guo², Yujiao Chen¹

¹Department of Occupational Health and Environmental Health, School of Public Health, Capital Medical University, Beijing 100069, PR China; Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing 100069, PR China.

|February 17, 2024

概括

N6-甲基氨酸 (m6A) 阅读器IGF2BP1对于的血液毒性至关重要. 它的减少表达通过影响RPL36稳定性而损害细胞增殖,但IGF2BP1过度表达提供了保护.

科学领域:

毒理学毒理学毒理学
表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.
分子生物学分子生物学

背景情况:

暴露会导致血液毒性,其中表观遗传修饰与其致病性有关.
N6-甲基氨酸 (m6A) 是一个关键的转录后修饰,但其在诱导的血液毒性中的作用尚不清楚.
m6A读者蛋白对于m6A介导的基因调节至关重要.

研究的目的:

为了研究m6A阅读器IGF2BP1在血毒性中的作用.
为了识别IGF2BP1的潜在m6A点,参与病原发生.
探索IGF2BP1和RPL36作为素诱导的造血损伤的潜在治疗点.

主要方法:

在暴露于的工人和细胞模型中评估IGF2BP1表达.
过度表达IGF2BP1在小鼠中,以评估其对暴露的保护作用.
进行了全转录组的m6A分析,以确定IGF2BP1的点.
分析了候选基因的mRNA表达和m6A甲基化,包括RPL36.
研究了IGF2BP1与RPL36mRNA结合的机制.

主要成果:

在暴露于的个体和细胞中,IGF2BP1的表达减少.
在小鼠中,IGF2BP1的过度表达保护了对诱导的造血损伤.
代谢物1,4-BQ改变了m6A的甲基化模式,导致低甲基化和减少Ribosomal Protein L36 (RPL36) 的表达.
减少了RPL36受损细胞增殖,IGF2BP1过度表达通过稳定RPL36mRNA扭转了这一效应.

结论:

m6A读者IGF2BP1在甲血毒性中起着保护作用.
IGF2BP1通过稳定RPL36mRNA来减轻素诱导的造血损伤,从而防止细胞增殖减少.
IGF2BP1和RPL36代表了治疗干预毒性治疗的有希望的分子标.

关键词:

暴露于二烯的情况血液中毒性血液中毒性在IGF2BP1中,我们可以使用IGF2BP1 N6 - 甲基氨酸 (m6A) 的使用.在RPL36中,我们可以使用RPL36.

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