Repair of potentially lethal damage in normal cells and ataxia telangiectasis cells; consideration of non-homologous end-joining
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- KAN'O Momoe
- Department of Radiology, School of Medicine, Keio University Department of Radiology, Graduate School of Medicine, Chiba University
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- KAWATA Tetsuya
- Department of Radiology, Graduate School of Medicine, Chiba University
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- ITO Hisao
- Department of Radiology, Graduate School of Medicine, Chiba University
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- SHIGEMATSU Naoyuki
- Department of Radiology, School of Medicine, Keio University
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- LIU Cuihua
- Department of Radiology, Graduate School of Medicine, Chiba University
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- UNO Takashi
- Department of Radiology, Graduate School of Medicine, Chiba University
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- ISOBE Kouich
- Department of Radiology, Graduate School of Medicine, Chiba University
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- KAWAKAMI Hiroyuki
- Department of Radiology, Graduate School of Medicine, Chiba University
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- CUCINOTTA Francis
- NASA Lyndon B Johnson Space Center, Radiation Biophysics Laboratory
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- GEORGE Kerry
- NASA Lyndon B Johnson Space Center, Radiation Biophysics Laboratory
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- KUBO Atsushi
- Department of Radiology, School of Medicine, Keio University
書誌事項
- タイトル別名
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- Repair of Potentially Lethal Damage in Normal Cells and Ataxia Telangiectasia Cells; Consideration of Non-Homologous End-Joining
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抄録
When cell lines are held in a quiescent state after irradiation, survival rates are greater than those from cells that are stimulated to grow immediately after irradiation. These differences in survival rates correspond to rates of potentially lethal damage repair. The effects of confluent holding recovery after γ-irradiation were investigated using normal human fibroblasts (AG1522) and ataxia telangiectasia fibroblasts (GM02052). Calyculin-A-induced premature chromosome condensation and fluorescent in situ hybridization were applied to study G2/M chromosomal aberrations. Survival results indicated normal capacity for PLDR in AG1522 cells but that PLDR was extremely compromised in GM02052 cells. The chromosomal aberration frequency decreased when AG1522 cells were allowed to repair for 24-h, whereas 24-hour incubation had little effect on the aberration frequency in GM02052 cells. Since the main mechanism for dsbs repair during G0/G1 phases of the cells cycle involve the non-homologous end-joining (NHEJ) process, our study indicates that for AG1522 cells the NHEJ repair process is more likely to induce accurate chromosome repair under quiescent G0 conditions than proliferating G1 phase, while in GM02052 cells the fidelity of NHEJ is similarly defective at either cell cycle phase. Reduced fidelity of NHEJ may be responsible for PLDR defect and its hyper-radiosensitivity in A-T cells.<br>
収録刊行物
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- Journal of Radiation Research
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Journal of Radiation Research 48 (1), 31-38, 2007
Journal of Radiation Research 編集委員会
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詳細情報 詳細情報について
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- CRID
- 1390001205216199424
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- NII論文ID
- 110006570514
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- NII書誌ID
- AA00705792
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- DOI
- 10.1269/jrr.0642
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- ISSN
- 13499157
- 04493060
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- NDL書誌ID
- 8748517
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
- Crossref
- NDL-Digital
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可