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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

Mechanism and repertoire of ASC-mediated gene expression

https://doi.org/10.24517/00027389
https://doi.org/10.24517/00027389
f4635632-a3dd-4461-a558-aa10691dd9a9
名前 / ファイル ライセンス アクション
CA-PR-SUDA-T-7655.pdf CA-PR-SUDA-T-7655.pdf (101.0 kB)
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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 Mechanism and repertoire of ASC-mediated gene expression
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 10.24517/00027389
ID登録タイプ JaLC
著者 Hasegawa, Mizuho

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WEKO 47615

Hasegawa, Mizuho

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Imamura, Ryu

× Imamura, Ryu

WEKO 256
e-Rad 10311680
金沢大学研究者情報 10311680
研究者番号 10311680

Imamura, Ryu

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Motani, Kou

× Motani, Kou

WEKO 47616

Motani, Kou

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Nishiuchi, Takumi

× Nishiuchi, Takumi

WEKO 302
e-Rad 20334790
金沢大学研究者情報 20334790
研究者番号 20334790

Nishiuchi, Takumi

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Matsumoto, Norihiko

× Matsumoto, Norihiko

WEKO 47617

Matsumoto, Norihiko

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Kinoshita, Takeshi

× Kinoshita, Takeshi

WEKO 478
金沢大学研究者情報 20311681
研究者番号 20311681

Kinoshita, Takeshi

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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 今村, 龍

× 今村, 龍

今村, 龍

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西内, 巧

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西内, 巧

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木下, 健

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木下, 健

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須田, 貴司

× 須田, 貴司

須田, 貴司

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提供者所属
内容記述タイプ Other
内容記述 金沢大学がん研究所
書誌情報 Journal of immunology

巻 182, 号 12, p. 7655-7662, 発行日 2009-06-15
ISSN
収録物識別子タイプ ISSN
収録物識別子 0022-1767
NCID
収録物識別子タイプ NCID
収録物識別子 AA00699656
DOI
関連タイプ isVersionOf
識別子タイプ DOI
関連識別子 10.4049/jimmunol.0800448
出版者
出版者 American Association of Immunologists
抄録
内容記述タイプ Abstract
内容記述 Apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC) is an adaptor molecule that mediates inflammatory and apoptotic signals. Although the role of ASC in caspase-1-mediated IL-1beta and IL-18 maturation is well known, ASC also induces NF-kappaB activation and cytokine gene expression in human cells. In this study, we investigated the molecular mechanism and repertoire of ASC-induced gene expression in human cells. We found that the specific activation of ASC induced AP-1 activity, which was required for optimal IL8 promoter activity. ASC activation also induced STAT3-, but not STAT1-, IFN-stimulated gene factor 3- or NF-AT-dependent reporter gene expression. The ASC-mediated AP-1 activation was NF-kappaB-independent and primarily cell-autonomous response, whereas the STAT3 activation required NF-kappaB activation and was mediated by a factor that can act in a paracrine manner. ASC-mediated AP-1 activation was inhibited by chemical or protein inhibitors for caspase-8, caspase-8-targeting small-interfering RNA, and p38 and JNK inhibitors, but not by a caspase-1 inhibitor, caspase-9 or Fas-associated death domain protein (FADD) dominant-negative mutants, FADD- or RICK-targeting small-interfering RNAs, or a MEK inhibitor, indicating that the ASC-induced AP-1 activation is mediated by caspase-8, p38, and JNK, but does not require caspase-1, caspase-9, FADD, RICK, or ERK. DNA microarray analyses identified 75 genes that were induced by ASC activation. A large proportion of them was related to transcription (23%), inflammation (21%), or cell death (16%), indicating that ASC is a potent inducer of inflammatory and cell death-related genes. This is the first report of ASC-mediated AP-1 activation and the repertoire of genes induced downstream of ASC activation.
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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