Selective and ATP-competitive kinesin KIF18A inhibitor suppresses the replication of influenza A virusopen access
- Authors
- Cho, Yong-Bin; Hong, Sungguan; Kang, Kyung-Won; Kang, Ji-Hun; Lee, Sang-Myeong; Seo, Young-Jin
- Issue Date
- May-2020
- Publisher
- Wiley-Blackwell
- Keywords
- influenza virus; KIF18A; RanBP3
- Citation
- Journal of Cellular and Molecular Medicine, v.24, no.10, pp 5463 - 5475
- Pages
- 13
- Journal Title
- Journal of Cellular and Molecular Medicine
- Volume
- 24
- Number
- 10
- Start Page
- 5463
- End Page
- 5475
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/41481
- DOI
- 10.1111/jcmm.15200
- ISSN
- 1582-1838
1582-4934
- Abstract
- The influenza virus is one of the major public health threats. However, the development of efficient vaccines and therapeutic drugs to combat this virus is greatly limited by its frequent genetic mutations. Because of this, targeting the host factors required for influenza virus replication may be a more effective strategy for inhibiting a broader spectrum of variants. Here, we demonstrated that inhibition of a motor protein kinesin family member 18A (KIF18A) suppresses the replication of the influenza A virus (IAV). The expression of KIF18A in host cells was increased following IAV infection. Intriguingly, treatment with the selective and ATP-competitive mitotic kinesin KIF18A inhibitor BTB-1 substantially decreased the expression of viral RNAs and proteins, and the production of infectious viral particles, while overexpression of KIF18A enhanced the replication of IAV. Importantly, BTB-1 treatment attenuated the activation of AKT, p38 MAPK, SAPK and Ran-binding protein 3 (RanBP3), which led to the prevention of the nuclear export of viral ribonucleoprotein complexes. Notably, administration of BTB-1 greatly improved the viability of IAV-infected mice. Collectively, our results unveiled a beneficial role of KIF18A in IAV replication, and thus, KIF18A could be a potential therapeutic target for the control of IAV infection. © 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd
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Collections - College of Natural Sciences > Department of Life Science > 1. Journal Articles
- College of Natural Sciences > Department of Chemistry > 1. Journal Articles
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