在细菌感染期间通过RNF213对脂聚糖的泛化
Elsje G Otten1, Emma Werner2, Ana Crespillo-Casado2
1MRC Laboratory of Molecular Biology, Cambridge, UK. gotten@mrc-lmb.cam.ac.uk.
Nature
|May 20, 2021
概括
不仅针对蛋白质,还针对细胞溶液中的细菌脂多糖 (LPS). 这一由RNF213调解的过程启动了抗菌自和细胞自主免疫.
科学领域:
- 细胞微生物学
- 免疫学
- 生物化学
背景情况:
- 随处可见化通常会改变蛋白质,标记细胞内细菌进行自.
- 在入侵细菌上存在的特定基质仍未确定.
研究的目的:
- 为了识别细胞质沙门氏菌的无处不在基质.
- 阐明RNF213在细菌无处不在和抗菌自中的作用.
主要方法:
- 通过使用E3泛素连接酶RNF213研究细菌脂聚糖 (LPS) 的无处不在.
- 分析了RNF213域在LPS无处不在和LUBAC招募中的功能.
- 评估了RNF213缺乏对细菌清除和自诱导的影响.
主要成果:
- 证明RNF213可在细胞质沙门氏菌上对脂质A部分产生无处不在作用.
- 显示RNF213对于产生细菌无素外层和招募LUBAC至关重要.
- 发现LPS的无处不在会触发抗菌自和细胞自主免疫.
结论:
- 化超越了蛋白质基质,包括LPS等非蛋白质分子.
- 通过RNF213对LPS的泛化是启动抗菌自的一个关键步骤.
- 这一发现扩大了对宿主防御机制的翻译后修改的理解.
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