相关实验视频
Updated: Jun 23, 2025

14:57
Yeast As a Chassis for Developing Functional Assays to Study Human P53
Published on: August 4, 2019
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在低氧条件下,p53 lysine-lactylated 修饰有助于 lipopolysaccharide 诱导的在 BV2 细胞中的前炎性激活
Xuechao Fei1, Lu Chen2, Jiayue Gao1
1Beijing Institute of Basic Medical Sciences, Beijing, 100850, China.
Neurochemistry international
|June 22, 2024
概括
在低氧状态下,p53氨酸乳化 (p53Kla) 会加剧微质细胞的炎症. 抑制乳酸生产可以通过向NF-κB通路来减少这种神经炎症损伤.
科学领域:
- 神经科学是一个神经科学.
- 免疫学 免疫学 免疫学
- 分子生物学分子生物学
背景情况:
- p53调节各种细胞过程,包括转录和增殖.
- p53和核因子-κB (NF-κB) 共同调节巨细胞中的炎症.
- 在缺氧下微质炎症中,p53氨酸乳化 (p53Kla) 的作用尚不清楚.
研究的目的:
- 调查缺氧加剧的微质炎症.
- 在这些条件下确定微质中的p53Kla水平.
- 阐明p53Kla在调解亲炎性表型中的作用.
主要方法:
- 使用的BV2微质细胞暴露于脂多糖 (LPS) 和缺氧 (Hy).
- 评估了p53和p53Kla蛋白水平和微质激活.
- 采用酸盐和突变的p53等离子体来研究p53Kla的影响.
主要成果:
- LPS-Hy显著增加了核和细胞质中的p53Kla,同时降低了p53水平.
- LPS-Hy激活了NF-κB通路,增加了化p65.5.
- 促炎性细胞因子表达 (iNOS,IL6,IL1β,TNFα) 和细胞毒性都增加了.
结论:
- 通过NF-κB通路,p53Kla通过缺氧促进LPS诱导的微质炎症.
- 抑制乳酸生产可能会减轻神经炎症损伤.
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