自依赖的拼接控制指导在衰老期间向炎症转化
Jaejin Kim1, Yeonghyeon Lee1, Taerang Jeon1
1School of Biological Sciences, Seoul National University, Seoul 08826, South Korea; Center for Systems Geroscience, Seoul National University, Seoul 08826, South Korea.
Developmental cell
|November 7, 2024
概括
自会通过降低拼接因子,改变RNA拼接,并促进炎症基因翻译来引导衰老期间的细胞炎症. 这一过程在人类的衰老和癌症中得到保护.
科学领域:
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
- 免疫学 免疫学 免疫学
背景情况:
- 细胞蛋白质和功能是由蛋白质组成决定的,在疾病中经常发生变化.
- 自,一种细胞降解过程,通过去除受损或不必要的蛋白质来塑造蛋白质组.
- RNA拼接变化是细胞衰老的特征,有助于病理状况.
研究的目的:
- 研究自在细胞衰老过程中调节转化体中的作用.
- 阐明自性影响老化中的替代拼接和炎症基因表达的机制.
- 探索这些途径在人类衰老和癌症中的保护.
主要方法:
- 系统的翻译形状,以分析衰老期间的全球翻译变化.
- 调查自对特定RNA拼接事件的影响,包括EIF4H外因子5跳转.
- 识别参与剪接调节器降解的自受体,例如SFPQ通过NBR1.1.
主要成果:
- 自会指导衰老特异性转化体促进炎症.
- 自调节衰老中的替代拼接,包括EIF4H外因子5跳转,这对炎症转化至关重要.
- 自选择性地通过NBR1受体降解拼接调节器SFPQ,从而促进这些拼接和转化变化.
结论:
- 自在需要时重塑细胞蛋白质组中发挥着关键作用,将选择性蛋白质降解与替代拼接联系起来,以驱动衰老中的炎症.
- 自,替代拼接和炎症翻译之间的相互作用是控制衰老和癌症中细胞功能的关键机制.
- 这些发现揭示了与人类组织衰老和癌症病原发生相关的自中心炎症控制.
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