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Updated: Feb 28, 2026

Monitoring eIF4F Assembly by Measuring eIF4E-eIF4G Interaction in Live Cells

Monitoring eIF4F Assembly by Measuring eIF4E-eIF4G Interaction in Live Cells

Published on: May 1, 2020

ASFV MGF110-7L 抑制eIF4G1通过内分泌网膜压力表达以阻止宿主翻译

Xinyu Gao¹, Suduo Jiang², Liyan Zhang¹

¹College of Life Science and Biotechnology, Heilongjiang Bayi Agricultural University, Daqing 163319, China.

|February 27, 2026

概括

非洲猪瘟病毒 (ASFV) 蛋白MGF110-7L通过降解eIF4G1通过压力颗粒和自来抑制宿主转化. 这揭示了一种新的ASFV免疫逃避策略和潜在的抗病毒点.

科学领域:

病毒学病毒学
分子生物学分子生物学
细胞生物学细胞生物学

背景情况:

非洲猪瘟病毒 (ASFV) 是一种致命的病毒,需要宿主转换进行复制和免疫逃避.
ASFV MGF110基因家族有未知功能的成员.
了解ASFV宿主相互作用机制对于开发抗病毒策略至关重要.

研究的目的:

研究ASFV MGF110-7L在调节宿主细胞转化中的作用.
阐明MGF110-7L影响蛋白质合成的分子机制.
为了确定ASFV干预的潜在目标.

主要方法:

利波基化试验测量新生的多合成.
西方涂抹用于评估翻译因子的蛋白质和mRNA水平.
抑制剂测定 (ISRIB,巴菲洛米辛A1) 来探测信号通路.
同免疫沉以研究蛋白质相互作用.

主要成果:

MGF110-7L以剂量和时间依赖的方式强烈抑制宿主转化.
MGF110-7L在转录后选择性地降低了eIF4G1蛋白水平,独立于mRNA变化.
ASFV MGF110-7L诱导了ER压力,促进了压力颗粒的形成,并通过自导致eIF4G1降解,涉及eIF4G1-G3BP1相互作用.

结论:

ASFV MGF110-7L通过通过压力颗粒促进eIF4G1的自性降解来抑制封顶依赖的翻译.
这代表了一种新的ASFV机制,用于控制宿主转换和逃避免疫反应.
这些发现提供了关于ASFV与宿主相互作用的见解,并表明了潜在的抗病毒点.

关键词:

非洲猪瘟病毒病毒细胞内膜网膜的压力应激单核细胞启动因子 4G1 主机翻译劫持主机翻译多基因家族的110-7L.

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