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TRIM39 negatively regulates the NFκB-mediated signaling pathway through stabilization of Cactin

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Title: TRIM39 negatively regulates the NFκB-mediated signaling pathway through stabilization of Cactin
Authors: Suzuki, Masanobu Browse this author
Watanabe, Masashi Browse this author
Nakamaru, Yuji Browse this author →KAKEN DB
Takagi, Dai Browse this author
Takahashi, Hidehisa Browse this author →KAKEN DB
Fukuda, Satoshi Browse this author →KAKEN DB
Hatakeyama, Shigetsugu Browse this author →KAKEN DB
Keywords: RelA/p65
Ubiquitin ligase
Issue Date: Mar-2016
Publisher: Springer
Journal Title: Cellular and molecular life sciences
Volume: 73
Issue: 5
Start Page: 1085
End Page: 1101
Publisher DOI: 10.1007/s00018-015-2040-x
PMID: 26363554
Abstract: NFκB is one of the central regulators of cell survival, immunity, inflammation, carcinogenesis and organogenesis. The activation of NFκB is strictly regulated by several posttranslational modifications including phosphorylation, neddylation and ubiquitination. Several types of ubiquitination play important roles in multi-step regulations of the NFκB pathway. Some of the tripartite motif-containing (TRIM) proteins functioning as E3 ubiquitin ligases are known to regulate various biological processes such as inflammatory signaling pathways. One of the TRIM family proteins, TRIM39, for which the gene has single nucleotide polymorphisms, has been identified as one of the genetic factors in Behcet's disease. However, the role of TRIM39 in inflammatory signaling had not been fully elucidated. In this study, to elucidate the function of TRIM39 in inflammatory signaling, we performed yeast two-hybrid screening using TRIM39 as a bait and identified Cactin, which has been reported to inhibit NFκB- and TLR-mediated transcriptions. We show that TRIM39 stabilizes Cactin protein and that Cactin is upregulated after TNFα stimulation. TRIM39 knockdown also causes activation of the NFκB signal. These findings suggest that TRIM39 negatively regulates the NFκB signal in collaboration with Cactin induced by inflammatory stimulants such as TNFα.
Rights: The final publication is available at Springer via
Type: article (author version)
Appears in Collections:医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 畠山 鎮次

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