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Mechanism and repertoire of ASC-mediated gene expression
https://doi.org/10.24517/00027389
https://doi.org/10.24517/00027389f4635632-a3dd-4461-a558-aa10691dd9a9
名前 / ファイル | ライセンス | アクション |
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CA-PR-SUDA-T-7655.pdf (101.0 kB)
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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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
× Hasegawa, Mizuho× Imamura, Ryu× Motani, Kou× Nishiuchi, Takumi× Matsumoto, Norihiko× Kinoshita, Takeshi× Suda, Takashi |
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著者別表示 |
今村, 龍
× 今村, 龍× 西内, 巧× 木下, 健× 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 |
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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 |