一个RBM10和NF-κB相互作用的宿主lncRNA促进JEV复制和神经元细胞死亡
Shraddha Tripathi1, Suryansh Sengar1, Bakhya Shree1
1Department of Biological Sciences, Birla Institute of Technology and Science, Pilani, Hyderabad Campus, Telangana, India.
Journal of virology
|November 22, 2023
概括
这项研究表明,JINR1长非编码RNA通过增加GRP78表达和激活NF-κB.通过增加GRP78表达和激活NF-κB.促进了黄病毒复制和神经元细胞死亡. 降低JINR1提供了一种潜在的治疗策略来对抗神经炎症.
科学领域:
- 神经科学是一个神经科学.
- 分子生物学分子生物学
- 病毒学 病毒学
背景情况:
- 像日本脑炎病毒这样的病毒会导致神经炎症和神经元损伤.
- 长非编码RNAs (lncRNAs) 在flavivirus诱导的神经毒性中的作用基本上是未知的.
研究的目的:
- 为了研究在感染期间神经元细胞中flavivirus诱导的lncRNA,JINR1的功能.
- 阐明JINR1对弗拉维病毒病原发生的分子机制.
主要方法:
- 感染神经元细胞中JINR1表达和功能的表征.
- 在JINR1耗尽后评估病毒复制和细胞死亡.
- 分析GRP78和RBM10表达及其与JINR1.1的相互作用.
- 对NF-κB通路激活的评估.
主要成果:
- JINR1的枯竭显著减少了病毒复制和神经元细胞死亡.
- 通过调节GRP78表达,JINR1促进病毒复制.
- 弗拉维病毒感染诱导RBM10,它与JINR1.1相互作用.
- 无论是RBM10还是JINR1,都会增强NF-κB的活性,从而导致细胞死亡.
结论:
- JINR1是弗拉维病毒诱导的神经炎症和神经元细胞死亡的关键媒介.
- JINR1促进病毒复制涉及GRP78的上调调节.
- JINR1-RBM10-NF-κB轴代表了弗拉维病毒神经毒性的关键途径.
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