Sendai virus V protein decreases nitric oxide production by inhibiting RIG-I signaling in infected RAW264.7 macrophages

Material type: 文書・図像類

Author: Morita, Naokoほか

Publisher: Elsevier

Publication date: 2020-02-05

Material Format: Digital

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Note (General)：: Sendai virus V protein is a known antagonist of RIG-I-like receptors (RLRs) RIG-I and MDA5, which activate transcription factors IRF3, leading to acti...

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Material Type: 文書・図像類
Title: Sendai virus V protein decreases nitric oxide production by inhibiting RIG-I signaling in infected RAW264.7 macrophages
Author/Editor: Morita, Naoko
Tanaka, Yukie
Odkhuu, Erdenezaya
Naiki, Yoshikazu
Komatsu, Takayuki
Koide, Naoki
Author Heading: Morita, Naoko
Tanaka, Yukie
Odkhuu, Erdenezaya
Naiki, Yoshikazu
Komatsu, Takayuki
Koide, Naoki
Publication, Distribution, etc.: Elsevier
Publication Date: 2020-02-05
Publication Date (W3CDTF): 2020-02-05
Alternative Title: Sendai virus V protein decreases nitric oxide production by inhibiting RIG-I signaling in infected RAW264.7 macrophages
Periodical title: Microbes and Infection
No. or year of volume/issue: 22 8
Volume: 22
Issue: 8
Pages: 322-330
ISSN (Periodical Title): ISSN : 1286-4579
Text Language Code: eng
Subject Heading: Sendai virus
V protein
Nitric oxide
RIG-I
TRIM25
Macrophages
Target Audience: 一般
Note (General): Sendai virus V protein is a known antagonist of RIG-I-like receptors (RLRs) RIG-I and MDA5, which activate transcription factors IRF3, leading to activation of ISGF3 and NF-kB. These transcription factors are known activators of inducible NO synthase (iNOS) and increase the production of nitric oxide (NO). By inhibiting ISGF3 and NF-kB, the V protein acts as an indirect negative regulator of iNOS and NO. Here we report that the V gene knockout Sendai virus [SeV V()] markedly enhanced iNOS expression and subsequent NO production in infected macrophages compared to wild-type SeV. The knockout of RIG-I in cells inhibited SeV V()-induced iNOS expression and subsequent NO production. To understand the underlying mechanism of the V protein-mediated negative regulation of iNOS activation, we transfected HEK293T cells with RIG-I and the RIG-I regulatory protein TRIM25. Our results demonstrated that the V protein inhibited iNOS activation via the RIG-I/TRIM25 pathway. Moreover, the V protein inhibited TRIM25-mediated K63-linked ubiquitination of RIG-I, as well as its CARD-dependent interaction with mitochondrial antiviral signaling (MAVS) molecules. These results suggest that the V protein downregulates iNOS activation and inhibits NO production by preventing the RIG-I-MAVS interaction, possibly through its effect on the ubiquitination status of RIG-I.
Source: https://u-fukui.repo.nii.ac.jp/?action=repository_action_common_download&item_id=28702&item_no=1&attribute_id=22&file_no=1
https://u-fukui.repo.nii.ac.jp/?action=repository_action_common_download&item_id=28702&item_no=1&attribute_id=22&file_no=1
Access Restrictions: 限定公開
Related Material (DOI): 10.1016/j.micinf.2020.01.005
Data Provider (Database): 国立情報学研究所 : 学術機関リポジトリデータベース（IRDB）（機関リポジトリ）
https://irdb.nii.ac.jp
Original Data Provider (Database): 福井大学 : 福井大学学術機関リポジトリ