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- 黒瀬 顕
- 岩手医科大学病理学第一講座
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- 田中 俊樹
- 山口大学大学院医学系研究科器官病態外科学呼吸器外科
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- 佐藤 雄一
- 岩手医科大学病理学第一講座 岩手医科大学脳神経外科学講座
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- 鎌滝 彰央
- 岩手医科大学病理学第一講座
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- 柴田 祐二
- 岩手医科大学病理学第一講座
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- 金 仁順
- 岩手医科大学病理学第一講座
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- Huang Xuan
- Brander Cancer Research Institute, New York Medical College
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- Darzynkiewicz Zbigniew
- Brander Cancer Research Institute, New York Medical College
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- 澤井 高志
- 岩手医科大学病理学第一講座
書誌事項
- タイトル別名
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- DNA damage and cell kinetics detected by cytometry: using phosphorylated histone H2AX as a marker of DNA double strand breaks
この論文をさがす
抄録
<p>Histone H2AX phosphorylated on Ser 139, defined as γH2AX, is a reporter of DNA double strand breaks (DSBs). While induction of DNA damage by genotoxic agents lead H2AX to γH2AX, it also is phosphorylated in unterated normal and tumor cells. The latter is designated as constitutive H2AX phosphorylation. We show here flow cytometric investigation of γH2AX in relation to cell cycle phase. Even in untreated exponentially growing HL-60 cells, γH2AX was detected during the cell cycle. Some of normal endothelial cells demonstrated dot-like positivity of γH2AX in their nuclei. Oxide-releasing aspirin induced DNA damage and it was attenuated in the presence of N-acetyl-L-cysteine, a scavenger of reactive oxigen species. A decrease in a cells’metabolic activity as a result of inhibition of glycolysis by 2-deoxy-D-glucose reduced DNA damage. Exposure of HL-60 cells to camptothecin led to phosphorylation of H2AX in S-phase cells. Four hours’exposure to camptothecin induced a cell population which had dramatically increased γH2AX immunofluorescence and corresponded to apoptosis. Inhibitors of DNA replication which are used to synchronize cultured cells in G1 phase caused DNA damage in S-phase cells and led to their apoptosis, i. e., the synchronization was caused by selective kill of S-phase cells through induction of DSBs. Moreover, synchronized cells in G1 phase showed DNA damage. Thus, detection of γH2AX immunohistochemically and cytometric investigation of it in relation to cell cycle phases is advantageous to estimate the effect of many agents causing DNA damage such as oxidative stress, metabolism or chemicals, and have a possibility to contribute significantly to elucidate carcinogenesis.</p>
収録刊行物
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- サイトメトリーリサーチ
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サイトメトリーリサーチ 17 (2), 25-30, 2007
日本サイトメトリー学会
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詳細情報 詳細情報について
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- CRID
- 1390001204472310656
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- NII論文ID
- 10019946299
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- NII書誌ID
- AN10356261
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- ISSN
- 24240664
- 09166920
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- 本文言語コード
- ja
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- データソース種別
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- JaLC
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可