文献类型： 外文期刊
作者： Zhu, Fang 1 ; Sheng, Xiangpeng 2 ; Yang, Fan 3 ; Wang, Xuechen 5 ; Yang, Cong 1 ; Ren, Jin 1 ; Wang, Chengcheng 1 ; Hu, Ronggui 1 ;
作者机构： 1.Guizhou Univ, Sch Med, Guiyang, Peoples R China
2.Chinese Acad Agr Sci, Harbin Vet Res Inst, State Key Lab Anim Dis Control & Prevent, Harbin, Peoples R China
3.Univ Chinese Acad Sci, Shanghai Inst Biochem & Cell Biol, Chinese Acad Sci, Ctr Excellence Mol Cell Sci,State Key Lab Mol Biol, Shanghai, Peoples R China
4.Zhejiang Univ, Affiliated Hosp 2, Liangzhu Lab, Sch Med, Hangzhou, Peoples R China
5.Shanghai Normal Univ, Coll Life Sci, Shanghai Key Lab Plant Mol Sci, Shanghai, Peoples R China
关键词： ER stress; HAX1; SARS-CoV-2; Spike; unfolded protein response
期刊名称：FEBS JOURNAL （ 影响因子：4.2； 五年影响因子：5.6 ）
ISSN： 1742-464X
年卷期： 2025 年
页码：
收录情况： SCI
摘要： SARS-CoV-2 continues to evolve with enhanced transmissibility, a feature primarily mediated by its spike (S) protein. While expression of the S protein in human cells can induce the accumulation of reactive oxygen species (ROS), the regulatory mechanisms governing this process remain poorly understood. Here, we identify the human protein HCLS1-associated protein X-1 (HAX1) as a key regulator that mitigates SARS-CoV-2S-induced ROS accumulation. A genome-wide screen revealed HAX1 as a binding partner of the SARS-CoV-2S protein in mammalian cells. HAX1 specifically interacts with the S1 subunit of S, and its deficiency effectively abolishes S-induced activation of endoplasmic reticulum (ER) stress responses, including the unfolded protein response (UPR). Notably, HAX1-dependent UPR activation is unique to SARS-CoV-2S and certain variants and is not triggered by other UPR inducers. Loss of HAX1 markedly exacerbates SARS-CoV-2S-induced ROS accumulation and mitochondrial dysfunction. Collectively, our findings uncover a previously unrecognized mechanism by which S modulates host stress responses and establish HAX1 as a host factor involved in SARS-CoV-2-related processes.
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