HAX1调解了宿主细胞中SARS-CoV-2尖端触发的展开蛋白质反应
Fang Zhu1, Xiangpeng Sheng2, Fan Yang3,4
1School of Medicine, Guizhou University, Guiyang, China.
The FEBS journal
|June 26, 2025
概括
人类蛋白质HAX1减轻了SARS-CoV-2尖端蛋白诱导的氧化压力. 失去HAX1会恶化反应性氧物种的积累和线粒体功能障碍,揭示病毒过程中的关键宿主因素.
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:
- SARS-CoV-2尖端蛋白增强了传染性,可以诱导人体细胞中的反应性氧物种 (ROS).
- 调节SARS-CoV-2尖端蛋白诱导的ROS积累的机制尚不清楚.
研究的目的:
- 为了确定调节SARS-CoV-2尖端蛋白诱导细胞压力的宿主因素.
- 阐明HAX1在减轻SARS-CoV-2尖端蛋白介导作用中的作用.
主要方法:
- 全基因组查以确定SARS-CoV-2尖端蛋白结合伙伴.
- 测试用于测量ROS积累和内质网膜 (ER) 应激反应.
- 研究HAX1缺乏对SARS-CoV-2尖端蛋白的细胞反应的影响.
主要成果:
- HAX1被确定为SARS-CoV-2尖端蛋白S1亚单元的结合伙伴.
- 缺少HAX1消除了尖端蛋白诱导的ER压力和展开的蛋白质反应 (UPR) 激活.
- HAX1的损失加剧了尖端蛋白诱导的ROS积累和线粒体功能障碍.
结论:
- HAX1作为一个关键的调节剂,减轻SARS-CoV-2尖端蛋白诱导的ROS积累和ER压力.
- HAX1-依赖的UPR激活是SARS-CoV-2尖端蛋白和某些变体的特征.
- HAX1是一种新型宿主因子,参与SARS-CoV-2的病变发生.
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