TRIM59 interacts with ECSIT and negatively regulates NF-κB and IRF-3/7-mediated signal pathways

Kondo, Takeshi; Watanabe, Masashi; Hatakeyama, Shigetsugu

Biochemical and Biophysical Research Communications, 2012, 422(3), 501-507

Permalink : https://hdl.handle.net/2115/49795

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アクセス権
open access
URI
https://hdl.handle.net/2115/49795
タイトル
TRIM59 interacts with ECSIT and negatively regulates NF-κB and IRF-3/7-mediated signal pathways
著者
Kondo, Takeshi ; Watanabe, Masashi ; Hatakeyama, Shigetsugu
e-Rad_Researcher
70333606
著者名
Kondo, Takeshi
著者名
Watanabe, Masashi
e-Rad_Researcher
70294973
著者名
Hatakeyama, Shigetsugu
言語
英語
キーワード
TRIM59
ECSIT
IPS-1
NF-κB
IRF
発行日
2012-06-08
出版者
Elsevier
収録物名
Biochemical and Biophysical Research Communications
巻(号)
422(3)
ページ
501-507
抄録
Innate immune responses are triggered by pathogen-associated molecular patterns (PAMPs) through pattern recognition receptors (PRRs) and then activate intracellular signaling pathways including NF-κB and interferon regulatory factors. Recently, it has been reported that tripartite motif (TRIM) proteins function as crucial regulators via ubiquitin-mediated modifications for these signaling pathways. In this study, we showed that one of the TRIM family ubiquitin ligases, TRIM59, interacts with ECSIT as an adaptor protein required for the TLR-mediated transduction pathway. Luciferase reporter assays using reporter plasmids including NF-κB responsive element, interferon β (IFN-β) promoter and interferon-sensitive response element (ISRE) showed that overexpression of TRIM59 repressed their transcriptional activities, whereas knockdown of TRIM59 enhanced their transcriptional activities. Furthermore, TRIM59 inhibited phosphorylation and dimerization of IRF3 and IRF7, suggesting that TRIM59 negatively regulates upstream kinases for IRFs. These findings indicate that TRIM59 may serve as a multifunctional regulator for innate immune signaling pathways.
資源タイプ
学術雑誌論文
出版タイプ
Accepted Manuscript
PISSN
0006-291X
関連情報
PMID
22588174
関連情報 (isVersionOf)
出版社版DOI
https://doi.org/10.1016/j.bbrc.2012.05.028