『徳島大学 教育・研究者情報データベース (EDB)』---[学外] /
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○種別 (必須): □学術論文 (審査論文) [継承]
○言語 (必須): □英語 [継承]
○招待 (推奨):
○審査 (推奨): □Peer Review [継承]
○カテゴリ (推奨):
○共著種別 (推奨):
○学究種別 (推奨):
○組織 (推奨):
○著者 (必須): 1. (英) Aoki Hiroki (日) (読)
○役割 (任意):
○貢献度 (任意):
○学籍番号 (推奨):
[継承]
2. (英) Kang M. Peter (日) (読)
○役割 (任意):
○貢献度 (任意):
○学籍番号 (推奨):
[継承]
3. (英) Hampe James (日) (読)
○役割 (任意):
○貢献度 (任意):
○学籍番号 (推奨):
[継承]
4. (英) Yoshimura Koichi (日) (読)
○役割 (任意):
○貢献度 (任意):
○学籍番号 (推奨):
[継承]
5.野間 隆文
○役割 (任意):
○貢献度 (任意):
○学籍番号 (推奨):
[継承]
6. (英) Matsuzaki Masunori (日) (読)
○役割 (任意):
○貢献度 (任意):
○学籍番号 (推奨):
[継承]
7. (英) Izumo Seigo (日) (読)
○役割 (任意):
○貢献度 (任意):
○学籍番号 (推奨):
[継承]
○題名 (必須): □(英) Direct activation of mitovhondrial apoptosis machinery by c-jun N-terminal kinase in adult cardiac myocytes  (日)    [継承]
○副題 (任意):
○要約 (任意): □(英) Although oxidative stress causes activation of c-Jun N-terminal kinase (JNK) and apoptosis in many cell types, how the JNK pathway is connected to the apoptosis pathway is unclear. The molecular mechanism of JNK-mediated apoptosis was investigated in adult rat cardiac myocytes in culture as a model system that is sensitive to oxidative stress. Oxidative stress caused JNK activation, cytochrome c release, and apoptosis without new protein synthesis. Oxidative stress-induced apoptosis was abrogated by dominant negative stress-activated protein kinase/extracellular signal-regulated kinase kinase-1 (SEK1)-mediated inhibition of the JNK pathway, whereas activation of the JNK pathway by constitutively active SEK1 was sufficient to cause apoptosis. Inhibition of caspase-9, an apical caspase in the mitochondrial apoptosis pathway, suppressed oxidative stress-induced apoptosis, whereas inhibition of caspase-8 had no effect, indicating that both the JNK pathway and the mitochondrial apoptosis machinery are central to oxidative stress-induced apoptosis. Both JNK and SEK1 localized on mitochondria where JNK was activated by oxidative stress. Furthermore, active JNK caused the release of apoptogenic factors such as cytochrome c from isolated mitochondria in a cell-free assay. These findings indicate that the JNK pathway is a direct activator of mitochondrial death machinery without other cellular components and provide a molecular linkage from oxidative stress to the mitochondrial apoptosis machinery.  (日)    [継承]
○キーワード (推奨): 1. (英) Adenoviridae (日) (読) [継承]
2. (英) Animals (日) (読) [継承]
3.アポトーシス (apoptosis) [継承]
4. (英) Blotting, Western (日) (読) [継承]
5. (英) Caspase 8 (日) (読) [継承]
6. (英) Caspase 9 (日) (読) [継承]
7. (英) Caspases (日) (読) [継承]
8.細胞死 (cell death) [継承]
9. (英) Cell-Free System (日) (読) [継承]
10. (英) Cells, Cultured (日) (読) [継承]
11. (英) Cytochrome c Group (日) (読) [継承]
12. (英) Cytosol (日) (読) [継承]
13. (英) Enzyme Activation (日) (読) [継承]
14.過酸化水素水 (hydrogen peroxide) [継承]
15. (英) In Situ Nick-End Labeling (日) (読) [継承]
16. (英) JNK Mitogen-Activated Protein Kinases (日) (読) [継承]
17. (英) MAP Kinase Signaling System (日) (読) [継承]
18. (英) Microscopy, Confocal (日) (読) [継承]
19. (英) Microscopy, Electron (日) (読) [継承]
20.ミトコンドリア (mitochondria) [継承]
21. (英) Mitogen-Activated Protein Kinase 8 (日) (読) [継承]
22. (英) Mitogen-Activated Protein Kinases (日) (読) [継承]
23.心筋 (myocardium) [継承]
24.酸化ストレス (oxidative stress) [継承]
25.リン酸化 (phosphorylation) [継承]
26. (英) Protein Binding (日) (読) [継承]
27. (英) Rats (日) (読) [継承]
28. (英) Recombinant Proteins (日) (読) [継承]
29. (英) Subcellular Fractions (日) (読) [継承]
30. (英) Time Factors (日) (読) [継承]
○発行所 (推奨): □The American Society for Biochemistry and Molecular Biology [継承]
○誌名 (必須): □The Journal of Biological Chemistry ([The American Society for Biochemistry and Molecular Biology])
(pISSN: 0021-9258, eISSN: 1083-351X)

○ISSN (任意): □0021-9258
ISSN: 0021-9258 (pISSN: 0021-9258, eISSN: 1083-351X)
Title: The Journal of biological chemistry
Title(ISO): J Biol Chem
Publisher: American Society for Biochemistry and Molecular Biology
 (NLM Catalog)   (Scopus)   (CrossRef)  (Scopus information is found. [need login])
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○巻 (必須): □277 [継承]
○号 (必須): □12 [継承]
○頁 (必須): □10244 10250 [継承]
○都市 (任意): □ワシントンDC (Washington, D.C./[アメリカ合衆国]) [継承]
○年月日 (必須): □西暦 2002年 3月 22日 (平成 14年 3月 22日) [継承]
○URL (任意): □http://www.jbc.org/cgi/content/abstract/277/12/10244 [継承]
○DOI (任意): □10.1074/jbc.M112355200    (→Scopusで検索) [継承]
○PMID (任意): □11786558    (→Scopusで検索) [継承]
○CRID (任意):
○WOS (任意):
○Scopus (任意): □2-s2.0-0037155837 [継承]
○評価値 (任意):
○被引用数 (任意):
○指導教員 (推奨):
○備考 (任意): 1.(英) Article.Affiliation: Department of Molecular Cardiovascular Biology, Yamaguchi University School of Medicine, Minami Kogushi, Ube, Yamaguchi 755-8505, Japan. haoki@po.cc.yamaguchi-u.ac.jp  (日)    [継承]
2.(英) Article.PublicationTypeList.PublicationType: Journal Article  (日)    [継承]
3.(英) Article.PublicationTypeList.PublicationType: Research Support, Non-U.S. Gov't  (日)    [継承]
4.(英) Article.PublicationTypeList.PublicationType: Research Support, U.S. Gov't, P.H.S.  (日)    [継承]

標準的な表示

和文冊子 ● Hiroki Aoki, Peter M. Kang, James Hampe, Koichi Yoshimura, Takafumi Noma, Masunori Matsuzaki and Seigo Izumo : Direct activation of mitovhondrial apoptosis machinery by c-jun N-terminal kinase in adult cardiac myocytes, The Journal of Biological Chemistry, Vol.277, No.12, 10244-10250, 2002.
欧文冊子 ● Hiroki Aoki, Peter M. Kang, James Hampe, Koichi Yoshimura, Takafumi Noma, Masunori Matsuzaki and Seigo Izumo : Direct activation of mitovhondrial apoptosis machinery by c-jun N-terminal kinase in adult cardiac myocytes, The Journal of Biological Chemistry, Vol.277, No.12, 10244-10250, 2002.

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