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| タイトル: | ASK1 restores the antiviral activity of APOBEC3G by disrupting HIV-1 Vif-mediated counteraction |
| 著者: | Miyakawa, Kei Matsunaga, Satoko Kanou, Kazuhiko Matsuzawa, Atsushi Morishita, Ryo Kudoh, Ayumi Shindo, Keisuke   https://orcid.org/0000-0001-8793-8189 (unconfirmed)Yokoyama, Masaru Sato, Hironori Kimura, Hirokazu Tamura, Tomohiko Yamamoto, Naoki Ichijo, Hidenori Takaori-Kondo, Akifumi Ryo, Akihide |
| 著者名の別形: | 高折, 晃史 |
| キーワード: | Biological sciences Immunology Microbiology Virology |
| 発行日: | 22-Apr-2015 |
| 出版者: | Nature Publishing Group |
| 誌名: | Nature Communications |
| 巻: | 6 |
| 論文番号: | 6945 |
| 抄録: | APOBEC3G (A3G) is an innate antiviral restriction factor that strongly inhibits the replication of human immunodeficiency virus type 1 (HIV-1). An HIV-1 accessory protein, Vif, hijacks the host ubiquitin-proteasome system to execute A3G degradation. Identification of the host pathways that obstruct the action of Vif could provide a new strategy for blocking viral replication. We demonstrate here that the host protein ASK1 (apoptosis signal-regulating kinase 1) interferes with the counteraction by Vif and revitalizes A3G-mediated viral restriction. ASK1 binds the BC-box of Vif, thereby disrupting the assembly of the Vif-ubiquitin ligase complex. Consequently, ASK1 stabilizes A3G and promotes its incorporation into viral particles, ultimately reducing viral infectivity. Furthermore, treatment with the antiretroviral drug AZT (zidovudine) induces ASK1 expression and restores the antiviral activity of A3G in HIV-1-infected cells. This study thus demonstrates a distinct function of ASK1 in restoring the host antiviral system that can be enhanced by AZT treatment. |
| 著作権等: | This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
| URI: | http://hdl.handle.net/2433/210234 |
| DOI(出版社版): | 10.1038/ncomms7945 |
| PubMed ID: | 25901786 |
| 出現コレクション: | 学術雑誌掲載論文等 |
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