转录因子JunB抑制C型肝炎病毒复制
Adi Ariffianto1, Lin Deng1, Saki Harada1
1Division of Infectious Disease Control, Center for Infectious Diseases, Kobe University Graduate School of Medicine, Kobe, Japan.
The Kobe journal of medical sciences
|September 4, 2023
概括
型肝炎病毒 (HCV) 感染激活了ROS/JNK通路,导致JunB酸化. JunB抑制HCV复制并导致铁代谢障碍,为HCV揭示了一个新的治疗点.
科学领域:
- 肝病学 肝病学是一种肝病学.
- 病毒学 病毒学
- 分子生物学分子生物学
背景情况:
- 型肝炎病毒 (HCV) 感染激活了活性氧物种 (ROS) /c-Jun N-终端激酶 (JNK) 信号通路.
- 简基因激活与肝脏疾病有关,包括新陈代谢障碍,肥胖症,肝硬化和肝细胞癌.
- 在HCV感染和发病过程中,JNK标基因JunB的作用尚不清楚.
研究的目的:
- 调查JunB酸化在HCV感染中的作用.
- 为了澄清JunB在HCV生命周期和相关的发病过程中的生理作用.
主要方法:
- 在Huh-7.5细胞的HCV J6/JFH1感染.
- 免疫块分析以检测JunB酸化.
- 小干扰RNA (siRNA) 的淘汰和JunB.的过度表达.
- 细胞内和细胞外HCVRNA和感染性标位的量化.
- 对肝素促进剂活性和mRNA水平的分析.
主要成果:
- 由HCV诱导的ROS/JNK激活促进了JunB酸化.
- JunB knockdown增加了细胞内HCVRNA和感染力.
- JunB过度表达减少了细胞内HCVRNA和感染力.
- JunB激活促进了肝素促进活性和mRNA水平.
结论:
- JunB可以抑制HCV的传播.
- 由HCV诱导的ROS/JNK/JunB信号通路在抑制HCV复制方面发挥着作用.
- JunB通过肝素的上调参与HCV介导的铁代谢障碍.
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