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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 | |||||||||||||
