Abstract |
The RIG-I receptor induces the innate antiviral responses upon sensing RNA viruses. The mechanisms through which RIG-I optimizes the strength of the downstream signaling remain incompletely understood. In this study, we identified that NSUN5 could potentiate the RIG-I innate signaling pathway. Deficiency of NSUN5 enhanced RNA virus proliferation and inhibited the induction of the downstream antiviral genes. Consistently, NSUN5-deficient mice were more susceptible to RNA virus infection than their wild-type littermates. Mechanistically, NSUN5 bound directly to both viral RNA and RIG-I, synergizing the recognition of dsRNA by RIG-I. Collectively, to our knowledge, this study characterized NSUN5 as a novel RIG-I coreceptor, playing a vital role in restricting RNA virus infection.
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Authors | Boyue Sun, Haoyang Zeng, Jiaqian Liang, Lele Zhang, Haiyang Hu, Quanyi Wang, Wei Meng, Chenhui Li, Fuqiang Ye, Chen Wang, Juanjuan Zhu |
Journal | Journal of immunology (Baltimore, Md. : 1950)
(J Immunol)
Vol. 205
Issue 12
Pg. 3408-3418
(12 15 2020)
ISSN: 1550-6606 [Electronic] United States |
PMID | 33177158
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | Copyright © 2020 by The American Association of Immunologists, Inc. |
Chemical References |
- Muscle Proteins
- RNA, Double-Stranded
- RNA, Viral
- Receptors, Immunologic
- Methyltransferases
- NSUN5 protein, human
- Nsun5 protein, mouse
- tRNA Methyltransferases
- DDX58 protein, human
- Ddx58 protein, mouse
- DEAD Box Protein 58
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Topics |
- Animals
- Chlorocebus aethiops
- DEAD Box Protein 58
(immunology)
- HEK293 Cells
- Humans
- Immunity, Innate
- Methyltransferases
(immunology)
- Mice
- Muscle Proteins
(immunology)
- RNA Virus Infections
(immunology)
- RNA Viruses
(immunology)
- RNA, Double-Stranded
(immunology)
- RNA, Viral
(immunology)
- Receptors, Immunologic
(immunology)
- Vero Cells
- tRNA Methyltransferases
(immunology)
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