Item type |
デフォルトアイテムタイプ(フル)(1) |
公開日 |
2020-06-02 |
タイトル |
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タイトル |
Gamma-interferon-inducible, lysosome/endosome-localized thiolreductase, GILT, has anti-retroviral activity and its expression is counteracted by HIV-1 |
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言語 |
en |
作成者 |
Kubo, Yoshinao
Izumida, Mai
Yashima, Yuka
Yoshii-Kamiyama, Haruka
Tanaka, Yuetsu
Yasui, Kiyoshi
Hayashi, Hideki
Matsuyama, Toshifumi
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アクセス権 |
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アクセス権 |
open access |
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アクセス権URI |
http://purl.org/coar/access_right/c_abf2 |
権利情報 |
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言語 |
en |
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権利情報 |
Creative Commons Attribution 3.0 |
権利情報 |
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言語 |
en |
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権利情報Resource |
https://creativecommons.org/licenses/by/3.0/ |
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権利情報 |
https://creativecommons.org/licenses/by/3.0/ |
主題 |
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言語 |
en |
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主題Scheme |
Other |
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主題 |
gamma-interferon |
主題 |
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言語 |
en |
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主題Scheme |
Other |
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主題 |
antiviral |
主題 |
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言語 |
en |
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主題Scheme |
Other |
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主題 |
endosome |
主題 |
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言語 |
en |
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主題Scheme |
Other |
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主題 |
retroviruses |
主題 |
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言語 |
en |
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主題Scheme |
Other |
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主題 |
thiolreductase |
内容記述 |
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内容記述タイプ |
Other |
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内容記述 |
The mechanism by which type II interferon (IFN) inhibits virus replications remains to be identified. Murine leukemia virus (MLV) replication was significantly restricted by γ-IFN, but not human immunodeficiency virus type 1 (HIV-1) replication. Because MLV enters host cells via endosomes, we speculated that certain cellular factors among γ-IFN-induced, endosome-localized proteins inhibit MLV replication. We found that γ-IFN-inducible lysosomal thiolreductase (GILT) significantly restricts HIV-1 replication as well as MLV replication by its thiolreductase activity. GILT silencing enhanced replication-defective HIV-1 vector infection and virion production in γ-IFN-treated cells, although γ-IFN did not inhibit HIV-1 replication. This result showed that GILT is required for the anti-viral activity of γ-IFN. Interestingly, GILT protein level was increased by γ-IFN in uninfected cells and env-deleted HIV-1-infected cells, but not in full-length HIV-1-infected cells. γ-IFN-induced transcription from the γ-IFN-activation sequence was attenuated by the HIV-1 Env protein. These results suggested that the γ-IFN cannot restrict HIV-1 replication due to the inhibition of γ-IFN signaling by HIV-1 Env. Finally, we found that 4,4’-dithiodipyridine (4-PDS), which inhibits S-S bond formation at acidic pH, significantly suppresses HIV-1 vector infection and virion production, like GILT. In conclusion, this study showed that GILT functions as a host restriction factor against the retroviruses, and a GILT mimic, 4-PDS, is the leading compound for the development of novel concept of anti-viral agents. |
内容記述 |
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内容記述タイプ |
Other |
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内容記述 |
論文 |
出版者 |
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言語 |
en |
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出版者 |
Impact Journals |
言語 |
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言語 |
eng |
資源タイプ |
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資源タイプ |
journal article |
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資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
出版タイプ |
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出版タイプ |
VoR |
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出版タイプResource |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
識別子 |
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識別子 |
http://hdl.handle.net/20.500.12000/45984 |
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識別子タイプ |
HDL |
関連情報 |
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識別子タイプ |
DOI |
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関連識別子 |
https://doi.org/10.18632/oncotarget.12104 |
関連情報 |
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識別子タイプ |
DOI |
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関連識別子 |
https://doi.org/10.18632/oncotarget.12104 |
収録物識別子 |
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収録物識別子タイプ |
ISSN |
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収録物識別子 |
1949-2553 |
収録物名 |
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言語 |
en |
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収録物名 |
Oncotarget |
書誌情報 |
巻 7,
号 44,
p. 71255-71273,
発行日 2016-09
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