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Caspase-8- and JNK-dependent AP-1 activation is required for Fas ligand-induced IL-8 production
https://doi.org/10.24517/00027363
https://doi.org/10.24517/000273637c36dd07-4c23-47a1-ac17-41e00adcadf6
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
CA-PR-SUDA-T-2376.pdf (817.3 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 | Caspase-8- and JNK-dependent AP-1 activation is required for Fas ligand-induced IL-8 production | |||||||||
| 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 | 10.24517/00027363 | |||||||||
| ID登録タイプ | JaLC | |||||||||
| 著者 |
Matsumoto, Norihiko
× Matsumoto, Norihiko× Imamura, Ryu× Suda, Takashi |
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| 著者別表示 |
今村, 龍
× 今村, 龍
× 須田, 貴司
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| 書誌情報 |
FEBS Journal 巻 279, 号 9, p. 2376-2384, 発行日 2007-03-01 |
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| ISSN | ||||||||||
| 収録物識別子タイプ | ISSN | |||||||||
| 収録物識別子 | 1742-464X | |||||||||
| DOI | ||||||||||
| 関連タイプ | isVersionOf | |||||||||
| 識別子タイプ | DOI | |||||||||
| 関連識別子 | 10.1111/j.1742-4658.2007.05772.x | |||||||||
| 出版者 | ||||||||||
| 出版者 | Blackwell Publishing | |||||||||
| 抄録 | ||||||||||
| 内容記述タイプ | Abstract | |||||||||
| 内容記述 | Despite a dogma that apoptosis does not induce inflammation, Fas ligand (FasL), a well-known death factor, possesses pro-inflammatory activity. For example, FasL induces nuclear factor κB (NF-κB) activity and interleukin 8 (IL-8) production by engagement of Fas in human cells. Here, we found that a dominant negative mutant of c-Jun, a component of the activator protein-1 (AP-1) transcription factor, inhibits FasL-induced AP-1 activity and IL-8 production in HEK293 cells. Selective inhibition of AP-1 did not affect NF-κB activation and vice versa, indicating that their activations were not sequential events. The FasL-induced AP-1 activation could be inhibited by deleting or introducing the lymphoproliferation (lpr)-type point mutation into the Fas death domain (DD), knocking down the Fas-associated DD protein (FADD), abrogating caspase-8 expression with small interfering RNAs, or using inhibitors for pan-caspase and caspase-8 but not caspase-1 or caspase-3. Furthermore, wildtype, but not a catalytically inactive mutant, of caspase-8 reconstituted the FasL-induced AP-1 activation in caspase-8-deficient cells. Fas ligand induced the phosphorylation of two of the three major mitogen-activated protein kinases (MAPKs): extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) but not p38 MAPK. Unexpectedly, an inhibitor for JNK but not for MAPK/ERK kinase inhibited the FasL-induced AP-1 activation and IL-8 production. These results demonstrate that FasL-induced AP-1 activation is required for optimal IL-8 production, and this process is mediated by FADD, caspase-8, and JNK. © 2007 The Authors. | |||||||||
| 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 | |||||||||
