慢性压力阻碍了压力颗粒的形成
Yuichiro Adachi1,2,3,4, Allison M Williams1,2, Masashi Masuda3
1Division of Rheumatology, Inflammation and Immunity, Brigham and Women's Hospital, Boston, MA, USA.
iScience
|January 26, 2026
概括
慢性压力通过导致核糖体停滞来阻止压力颗粒的形成. 这种核糖体停滞阻碍了多元体的分解,即使细胞面临急性压力.
科学领域:
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
- 压力反应应对压力.
背景情况:
- 压力颗粒 (SG) 是在急性压力期间形成的细胞质焦点.
- SG形成涉及mRNA翻译抑制和多元体分解.
- 在慢性压力下SG的动态仍然不太清楚.
研究的目的:
- 在慢性压力下调查SG组件和动态.
- 阐明慢性压力后SG形成失败背后的分子机制.
主要方法:
- 细胞预条件与慢性低剂量压力.
- 在急性压力应用.
- 蛋白质合成试验. 蛋白质合成试验.
- 多种体概况. 多种体概况.
- 对翻译延长因子eEF2酸化的分析.
主要成果:
- 慢性压力预先调节会在急性压力时抑制SG组合.
- 蛋白质合成减少,但多体部分保存.
- 慢性压力会通过eEF2酸化诱导核糖体停滞.
- 核糖体阻滞在机理上不同于核糖体碰撞.
结论:
- 慢性压力会导致核糖体停滞,损害多核糖体的分解.
- 这种核糖体延迟会在随后的急性压力时防止压力颗粒的形成.
- 研究结果揭示了在转化层面应激适应的新机制.
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