African swine fever virus infection regulates pyroptosis by cleaving gasdermin A via active caspase-3 and caspase-4

文献类型： 外文期刊

第一作者： Li, Shuai

作者： Li, Shuai;Song, Jie;Liu, Jia;Zhou, Shijun;Zhao, Gaihong;Li, Tingting;Huang, Li;Li, Jiangnan;Weng, Changjiang;Li, Shuai;Song, Jie;Liu, Jia;Zhou, Shijun;Zhao, Gaihong;Li, Tingting;Huang, Li;Li, Jiangnan;Weng, Changjiang

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期刊名称：JOURNAL OF BIOLOGICAL CHEMISTRY （ 影响因子：3.9； 五年影响因子：4.3 ）

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年卷期： 2024 年 300 卷 6 期

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收录情况： SCI

摘要： African swine fever, caused by the African swine fever virus (ASFV), is a viral hemorrhagic disease that affects domestic pigs and wild boars. ASFV infection causes extensive tissue damage, and the associated mechanism is poorly understood. Pyroptosis is characterized by the activation of inflammatory caspases and pore formation in the cellular plasma membrane, resulting in the release of inflammatory cytokines and cell damage. How ASFV infection regulates pyroptosis remains unclear. Here, using siRNA assay and overexpression methods, we report that ASFV infection regulated pyroptosis by cleaving the pyroptosis execution protein gasdermin A (GSDMA). ASFV infection activated caspase-3 and caspase-4, which specifically cleaved GSDMA at D75-P76 and D241-V242 to produce GSDMA into five fragments, including GSDMA-N1-75, GSDMA-N1-241, and GSDMA-N76-241 fragments at the N-terminal end of GSDMA. Only GSDMA-N1-241, which was produced in the late stage of ASFV infection, triggered pyroptosis and inhibited ASFV replication. The fragments, GSDMA-N1-75 and GSDMA-N76-241, lose the ability to induce pyroptosis. anism for the regulation of pyroptosis.

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