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  1. H-1. がん進展制御研究所
  2. h-1 10. 学術雑誌掲載論文
  3. 1. 査読済論文

Vitamin B6 Prevents IL-1β Protein Production by Inhibiting NLRP3 Inflammasome Activation

https://doi.org/10.24517/00027494
https://doi.org/10.24517/00027494
e42f4a0e-d0fc-40ee-a297-04b3e8efee4e
名前 / ファイル ライセンス アクション
CA-PR-SUDA-T-24517.pdf CA-PR-SUDA-T-24517.pdf (2.5 MB)
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Item type 学術雑誌論文 / Journal Article(1)
公開日 2017-10-05
タイトル
タイトル Vitamin B6 Prevents IL-1β Protein Production by Inhibiting NLRP3 Inflammasome Activation
言語
言語 eng
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_6501
資源タイプ journal article
ID登録
ID登録 10.24517/00027494
ID登録タイプ JaLC
著者 Zhang, Peipei

× Zhang, Peipei

WEKO 47948

Zhang, Peipei

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Tsuchiya, Kohsuke

× Tsuchiya, Kohsuke

WEKO 47949
金沢大学研究者情報 50437216
研究者番号 50437216

Tsuchiya, Kohsuke

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Kinoshita, Takeshi

× Kinoshita, Takeshi

WEKO 47950
e-Rad 20311681

Kinoshita, Takeshi

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Kushiyama, Hiroko

× Kushiyama, Hiroko

WEKO 47951

Kushiyama, Hiroko

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Suidasari, Sofya

× Suidasari, Sofya

WEKO 47952

Suidasari, Sofya

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Hatakeyama, Mizuki

× Hatakeyama, Mizuki

WEKO 47953

Hatakeyama, Mizuki

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Imura, Hisanori

× Imura, Hisanori

WEKO 60
金沢大学研究者情報 60142923
研究者番号 60142923

Imura, Hisanori

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Kato, Norihisa

× Kato, Norihisa

WEKO 47954

Kato, Norihisa

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Suda, Takashi

× Suda, Takashi

WEKO 83
e-Rad 70250090
金沢大学研究者情報 70250090
研究者番号 70250090

Suda, Takashi

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著者別表示 土屋, 晃介

× 土屋, 晃介

土屋, 晃介

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木下, 健

× 木下, 健

木下, 健

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井村, 久則

× 井村, 久則

井村, 久則

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須田, 貴司

× 須田, 貴司

須田, 貴司

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書誌情報 Journal of Biological Chemistry

巻 291, 号 47, p. 24517-24527, 発行日 2016-11-18
ISSN
収録物識別子タイプ ISSN
収録物識別子 0021-9258
NCID
収録物識別子タイプ NCID
収録物識別子 AA00251083
DOI
関連タイプ isVersionOf
識別子タイプ DOI
関連識別子 10.1074/jbc.M116.743815
出版者
出版者 American Society for Biochemistry and Molecular Biology
抄録
内容記述タイプ Abstract
内容記述 Vitamin B6 includes six water-soluble vitamers: pyridoxal (PL), pyridoxamine (PM), pyridoxine (PN), and their phosphorylated forms. Pyridoxal 5o'-phosphate (PLP) is an important cofactor for many metabolic enzymes. Several lines of evidence demonstrate that blood levels of PLP are significantly lower in patients with inflammation than in control subjects and that vitamin B6 has anti-inflammatory effects, with therapeutic potential for a variety of inflammatory diseases. Although one of our group previously demonstrated that PL inhibits the NF-κB pathway, the molecular mechanism by which vitamin B6 suppresses inflammation is not well understood. Here, we showed that both PL and PLP suppressed the expression of cytokine genes in macrophages by inhibiting Toll-like receptor (TLR)-mediated TAK1 phosphorylation and the subsequent NF-κB and JNK activation. Furthermore, PL and PLP abolished NLRP3-dependent caspase-1 processing and the subsequent secretion of mature IL-1β and IL-18 in LPS-primed macrophages. In contrast, PM and PN had little effect on IL-1β production. PLP, but not PL, markedly reduced the production of mitochondrial reactive oxygen species (ROS) in peritoneal macrophages. Importantly, PL and PLP reduced IL-1β production induced by LPS and ATP, or by LPS alone, in mice. Moreover, PL and PLP protected mice from lethal endotoxic shock. Collectively, these findings reveal novel anti-inflammatory activities for vitamin B6 and suggest its potential for preventing inflammatory diseases driven by the NLRP3 inflammasome. © 2016 by The American Society for Biochemistry and Molecular Biology, Inc.
権利
権利情報 © 2016 by The American Society for Biochemistry and Molecular Biology, Inc.
著者版フラグ
出版タイプ AM
出版タイプResource http://purl.org/coar/version/c_ab4af688f83e57aa
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