Identification of STAU1 as a regulator of HBV replication by TurboID-based proximity labeling.

Identification of STAU1 as a regulator of HBV replication by TurboID-based proximity labeling.
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通过基于 TurboID 的邻近标记鉴定 STAU1 作为 HBV 复制的调节因子

DOI:
10.1016/j.isci.2022.104416
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发表时间:
2022-06-17
期刊:
影响因子:
5.8
通讯作者:
Hu, Jie-Li
Hu, Jie-Li
中科院分区:
综合性期刊2区
文献类型:
--
作者:
Wei, Xia-Fei;Fan, Shu-Ying;Wang, Yu-Wei;Li, Shan;Long, Shao-Yuan;Gan, Chun-Yang;Li, Jie;Sun, Yu-Xue;Guo, Lin;Wang, Pei-Yun;Yang, Xue;Wang, Jin-Lan;Cui, Jing;Zhang, Wen-Lu;Huang, Ai-Long;Hu, Jie-Li

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The core promoter (CP) of hepatitis B virus (HBV) is critical for HBV replication by controlling the transcription of pregenomic RNA (pgRNA). Host factors regulating the activity of the CP can be identified by different methods. Biotin-based proximity labeling, a powerful method with the capability to capture weak or dynamic interactions, has not yet been used to map proteins interacting with the CP. Here, we established a strategy, based on the newly evolved promiscuous enzyme TurboID, for interrogating host factors regulating the activity of HBV CP. Using this strategy, we identified STAU1 as an important factor involved in the regulation of HBV CP. Mechanistically, STAU1 indirectly binds to CP mediated by TARDBP, and recruits the SAGA transcription coactivator complex to the CP to upregulate its activity. Moreover, STAU1 binds to HBx and enhances the level of HBx by stabilizing it in a ubiquitin-independent manner. HBV core promoter binding factors were interrogated by a proximity labeling method STAU1 enhances HBV transcription and replication STAU1 indirectly binds to core promoter via TARDBP and recruits SAGA complex STAU1 binds to HBx and increases its stability Molecular biology; Virology
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