人类细胞巨型病毒感染通过依赖UL38的mTOR-KAP1通路诱导L1的表达
Sehong Park1,2,3, Jiseok Jeong1,2,3, Kwangseog Ahn1,2,3
1Center for RNA Research, Institute for Basic Science, Seoul, Republic of Korea.
PloS one
|April 23, 2025
概括
人类细胞巨型病毒 (HCMV) 通过通过mTOR介导的酸化,通过非活性化表观遗传抑制剂KAP1来提高LINE-1 (L1) 表达的调节. 这种相互作用促进了HCMVDNA复制和病毒传播.
科学领域:
- 病毒学 病毒学
- 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:
- 人类细胞巨型病毒 (HCMV) 和LINE-1 (L1) 逆转移素在宿主细胞内共存.
- HCMV通过升级L1表达来增强自身的DNA复制和生命周期.
- 这种由HCMV介导的L1上调的机制以前是未知的.
研究的目的:
- 阐明HCMV增加L1表达的分子机制.
- 研究KRAB相关蛋白1 (KAP1) 在HCMV诱导的L1上调中的作用.
- 在HCMV感染期间识别调节mTOR-KAP1通路的病毒因素.
主要方法:
- 细胞培养和HCMV感染模型.
- 西部涂抹检测KAP1酸化.
- 染色体可访问性测试用于评估L1促进剂活性.
- 用mTOR抑制剂治疗和对HCMV突变的分析 (UL38).
主要成果:
- HCMV感染在S824酸化了KAP1,降低了其抑制功能.
- 这种酸化增加了L1促进体的染色质可访问性.
- 由HCMV激活mTOR激酶驱动KAP1酸化和L1表达.
- HCMV UL38蛋白对于激活mTOR-KAP1通路和L1上调是必不可少的.
结论:
- 型冠状病毒感染通过mTOR介导的酸化功能性地使表观遗传抑制剂KAP1失活.
- HCMV UL38蛋白质作为一个关键的病毒调节剂,激活mTOR-KAP1通路,以调节L1表达.
- 这种HCMV和L1之间的协同相互作用对于病毒复制至关重要.
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