成熟 microRNA 结合蛋白 QKI 可抑制细胞外 microRNA let-7b 的释放。

IF 3.3 3区 生物学 Q3 CELL BIOLOGY
Journal of cell science Pub Date : 2024-11-01 Epub Date: 2024-11-06 DOI:10.1242/jcs.261575
Kyung-Won Min, Kyoung-Min Choi, Hyejin Mun, Seungbeom Ko, Ji Won Lee, Cari A Sagum, Mark T Bedford, Young-Kook Kim, Joe R Delaney, Jung-Hyun Cho, Ted M Dawson, Valina L Dawson, Waleed Twal, Dong-Chan Kim, Clarisse H Panganiban, Hainan Lang, Xin Zhou, Seula Shin, Jian Hu, Tilman Heise, Sang-Ho Kwon, Dongsan Kim, Young Hwa Kim, Sung-Ung Kang, Kyungmin Kim, Sydney Lewis, Ahmet Eroglu, Seonghyun Ryu, Dongin Kim, Jeong Ho Chang, Junyang Jung, Je-Hyun Yoon
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引用次数: 0

摘要

Argonaute(AGO)是 RNA 诱导的沉默复合体(RISC)的一个组成部分,是一种具有代表性的 RNA 结合蛋白(RBP),已知能与成熟的微 RNA(miRNA)结合,直接参与转录后基因沉默。然而,尽管 miRNA 具有重要的生物学意义,但其他微 RNA 结合蛋白(miRBPs)在调控 miRNA 装载、与 RISC 分离和细胞外释放方面的作用仍不清楚。在这项研究中,我们用蛋白质阵列分析了miRBPs,并鉴定了118个与miRNA直接结合的RNA结合蛋白。在这些蛋白中,RBP quaking(QKI)通过控制额外的 miRBPs(如 hnRNPD/AUF1 和 hnRNPK)将 let-7b 装入胞外囊泡,从而抑制成熟 microRNA let-7b 的胞外释放。QKI 耗竭后,let-7b 的细胞外释放增强,激活了 Toll 样受体 7(TLR7),促进受体细胞产生促炎细胞因子,导致小鼠大脑皮层发炎。因此,本研究揭示了 QKI 通过调节细胞外 let-7b 的释放对抑制脑部炎症的贡献。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Mature microRNA-binding protein QKI suppresses extracellular microRNA let-7b release.

Argonaute (AGO), a component of RNA-induced silencing complexes (RISCs), is a representative RNA-binding protein (RBP) known to bind with mature microRNAs (miRNAs) and is directly involved in post-transcriptional gene silencing. However, despite the biological significance of miRNAs, the roles of other miRNA-binding proteins (miRBPs) remain unclear in the regulation of miRNA loading, dissociation from RISCs and extracellular release. In this study, we performed protein arrays to profile miRBPs and identify 118 RBPs that directly bind to miRNAs. Among those proteins, the RBP quaking (QKI) inhibits extracellular release of the mature microRNA let-7b by controlling the loading of let-7b into extracellular vesicles via additional miRBPs such as AUF1 (also known as hnRNPD) and hnRNPK. The enhanced extracellular release of let-7b after QKI depletion activates Toll-like receptor 7 (TLR7) and promotes the production of proinflammatory cytokines in recipient cells, leading to brain inflammation in the mouse cortex. Thus, this study reveals the contribution of QKI to the inhibition of brain inflammation via regulation of extracellular let-7b release.

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来源期刊
Journal of cell science
Journal of cell science 生物-细胞生物学
CiteScore
7.30
自引率
2.50%
发文量
393
审稿时长
1.4 months
期刊介绍: Journal of Cell Science publishes cutting-edge science, encompassing all aspects of cell biology.
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