Transcriptome Analysis of Retinoic Acid-Inducible Gene I Overexpression Reveals the Potential Genes for Autophagy-Related Negative Regulation
文献类型: 外文期刊
第一作者: Ye, Shaotang
作者: Ye, Shaotang;Wang, Ji;Li, Qi;Xu, Liang;Wang, Zhen;Mao, Jianwei;Wang, Jingyu;Cheng, Kui;Chen, Aolei;Zhou, Pei;Li, Shoujun;Ye, Shaotang;Wang, Ji;Li, Qi;Xu, Liang;Wang, Zhen;Mao, Jianwei;Wang, Jingyu;Cheng, Kui;Chen, Aolei;Zhou, Pei;Li, Shoujun;Ye, Shaotang;Wang, Ji;Li, Qi;Xu, Liang;Wang, Zhen;Mao, Jianwei;Wang, Jingyu;Cheng, Kui;Chen, Aolei;Zhou, Pei;Li, Shoujun;Tan, Chen;Tan, Chen;Yang, Xiaoyun
作者机构:
关键词: RIG-I; overexpression; autophagy; negative regulation; transcriptome analysis
期刊名称:CELLS ( 影响因子:7.666; 五年影响因子:7.677 )
ISSN:
年卷期: 2022 年 11 卷 13 期
页码:
收录情况: SCI
摘要: Retinoic acid-inducible gene I (RIG-I) serves as an essential viral RNA sensor for innate immune. The activation of the RIG-I-like receptors (RLRs) pathway triggers many regulations for the outcome of type I interferon, including ubiquitination, dephosphorylation, ISGylation, and autophagy. However, the autophagy-related regulation of RIG-I is still not fully understood. To investigate the potentially unknown genes related to autophagy-related regulation of RIG-I, we firstly confirm the induction of autophagy derived by overexpression of RIG-I. Furthermore, the autophagy inducer and inhibitor drugs were used in different assays. The results showed autophagy could control the activation of RLRs pathway and expression of exogenous RIG-I. In addition, we carried out the transcriptome analysis of overexpression of RIG-I in vitro. Differentially expressed genes (DEGs) in GO and KEGG signaling pathways enrichment provided a newly complex network. Finally, the validation of qPCR indicated that the DEGs PTPN22, PRKN, OTUD7B, and SIRT2 were correlated to the negative regulation of excessive expression of RIG-I. Taken together, our study contributed new insights into a more comprehensive understanding of the regulation of excessive expression of RIG-I. It provided the potential candidate genes for autophagy-related negative regulation for further investigation.
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