Item type |
デフォルトアイテムタイプ(フル)(1) |
公開日 |
2007-03-08 |
タイトル |
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タイトル |
Inhibition of heat shock protein-90 modulates multiple functions required for survival of human T-cell leukemia virus type I-infected T-cell lines and adult T-cell leukemia cells |
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言語 |
en |
作成者 |
Kawakami, Hirochika
Tomita, Mariko
Okudaira, Taeko
Chie, Ishikawa
Matsuda, Takehiro
Tanaka, Yuetsu
Nakazato, Tetsuro
Taira, Naoya
Ohshiro, Kazuiku
Mori, Naoki
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アクセス権 |
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アクセス権 |
open access |
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アクセス権URI |
http://purl.org/coar/access_right/c_abf2 |
権利情報 |
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言語 |
en |
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権利情報 |
Copyright (c) 2007 Wiley-Liss, Inc |
主題 |
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言語 |
en |
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主題Scheme |
Other |
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主題 |
ATL |
主題 |
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言語 |
en |
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主題Scheme |
Other |
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主題 |
HTLV-I |
主題 |
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言語 |
en |
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主題Scheme |
Other |
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主題 |
17-AAG |
主題 |
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言語 |
en |
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主題Scheme |
Other |
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主題 |
Hsp90 |
主題 |
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言語 |
en |
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主題Scheme |
Other |
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主題 |
client protein |
内容記述 |
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内容記述タイプ |
Other |
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内容記述 |
The molecular chaperone Hsp90 is involved in the stabilization and conformational maturation of many signaling proteins that are deregulated in cancers. The geldanamycin derivative 17-AAG is currently tested in clinical trials and known to inhibit the function of Hsp90 and promote the proteasomal degradation of its misfolded client proteins. ATL is a fatal malignancy of T lymphocytes caused by HTLV-I infection and remains incurable. Since Hsp90 is overexpressed in HTLV-I-infected T-cell lines and primary ATL cells, we analyzed the effects of 17-AAG on cell survival, apoptosis and expression of signal transduction proteins. HTLV-I-infected T-cell lines and primary ATL cells were significantly more sensitive to 17-AAG in cell survival assays than normal PBMCs. 17-AAG induced the inhibition of cell cycle and apoptosis. These effects could be mediated by inactivation of NF-B, AP-1 and PI3K/Akt pathways, as well as reduction of expression of proteins involved in the G1-S cell cycle transition and apoptosis. Proteasome inhibition interfered with 17-AAG-mediated signaling proteins depletion. Collectively, our results indicate that 17-AAG suppresses ATL cell survival through, at least in part, destabilization of several client proteins and suggest that 17-AAG is a potentially useful chemotherapeutic agent for ATL. |
内容記述 |
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内容記述タイプ |
Other |
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内容記述 |
論文 |
出版者 |
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言語 |
en |
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出版者 |
Wiley-Liss, Inc. |
言語 |
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言語 |
eng |
資源タイプ |
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資源タイプ |
journal article |
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資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
出版タイプ |
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出版タイプ |
AM |
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出版タイプResource |
http://purl.org/coar/version/c_ab4af688f83e57aa |
識別子 |
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識別子 |
http://hdl.handle.net/20.500.12000/271 |
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識別子タイプ |
HDL |
関連情報 |
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識別子タイプ |
DOI |
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関連識別子 |
10.1002/ijc.22403 |
収録物識別子 |
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収録物識別子タイプ |
ISSN |
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収録物識別子 |
00207136 |
収録物識別子 |
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収録物識別子タイプ |
NCID |
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収録物識別子 |
AA00680002 |
収録物名 |
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言語 |
en |
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収録物名 |
International Journal of Cancer |
書誌情報 |
巻 120,
号 8,
p. 1811-1820,
発行日 2007-01
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