Communications Biology (May 2022)
SARS-CoV-2 ORF6 disrupts nucleocytoplasmic trafficking to advance viral replication
- Yoichi Miyamoto,
- Yumi Itoh,
- Tatsuya Suzuki,
- Tomohisa Tanaka,
- Yusuke Sakai,
- Masaru Koido,
- Chiaki Hata,
- Cai-Xia Wang,
- Mayumi Otani,
- Kohji Moriishi,
- Taro Tachibana,
- Yoichiro Kamatani,
- Yoshihiro Yoneda,
- Toru Okamoto,
- Masahiro Oka
Affiliations
- Yoichi Miyamoto
- Laboratory of Nuclear Transport Dynamics, National Institutes of Biomedical Innovation, Health and Nutrition (NIBIOHN)
- Yumi Itoh
- Institute for Advanced Co-Creation Studies, Research Institute for Microbial Diseases, Osaka University
- Tatsuya Suzuki
- Institute for Advanced Co-Creation Studies, Research Institute for Microbial Diseases, Osaka University
- Tomohisa Tanaka
- Department of Microbiology, Graduate School of Medicine, University of Yamanashi
- Yusuke Sakai
- Department of Pathology, National Institute of Infectious Diseases
- Masaru Koido
- Department of Cancer Biology, Institute of Medical Science, The University of Tokyo
- Chiaki Hata
- Cell Engineering Corporation
- Cai-Xia Wang
- Cell Engineering Corporation
- Mayumi Otani
- Laboratory of Nuclear Transport Dynamics, National Institutes of Biomedical Innovation, Health and Nutrition (NIBIOHN)
- Kohji Moriishi
- Department of Microbiology, Graduate School of Medicine, University of Yamanashi
- Taro Tachibana
- Cell Engineering Corporation
- Yoichiro Kamatani
- Department of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo
- Yoshihiro Yoneda
- National Institutes of Biomedical Innovation, Health and Nutrition (NIBIOHN)
- Toru Okamoto
- Institute for Advanced Co-Creation Studies, Research Institute for Microbial Diseases, Osaka University
- Masahiro Oka
- Laboratory of Nuclear Transport Dynamics, National Institutes of Biomedical Innovation, Health and Nutrition (NIBIOHN)
- DOI
- https://doi.org/10.1038/s42003-022-03427-4
- Journal volume & issue
-
Vol. 5,
no. 1
pp. 1 – 15
Abstract
The SARS-CoV-2 ORF6, an antagonist of interferon-mediated antiviral signaling, directly binds to STAT1 and prevents its nuclear localization.
