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Differential role of repair proteins, BRCA1/NBS1 and Ku70/DNA-PKcs, in radiation-induced centrosome overduplication
https://repo.qst.go.jp/records/45979
https://repo.qst.go.jp/records/45979d94c0e72-af04-4893-ae39-45770db11d9e
| Item type | 学術雑誌論文 / Journal Article(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 2011-01-04 | |||||
| タイトル | ||||||
| タイトル | Differential role of repair proteins, BRCA1/NBS1 and Ku70/DNA-PKcs, in radiation-induced centrosome overduplication | |||||
| 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 | |||||
| アクセス権 | ||||||
| アクセス権 | metadata only access | |||||
| アクセス権URI | http://purl.org/coar/access_right/c_14cb | |||||
| 著者 |
Shimada, Mikio
× Shimada, Mikio× Kobayashi, Jyunya× Hirayama, Ryoichi× Komatsu, Kenshi× 島田 幹男× 小林 純也× 平山 亮一× 小松 賢志 |
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| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | Centrosomes are important cytoplasmic organelles involved in chromosome segregation, defects in which can result in aneuploidy, and contribute to tumorigenesis. It is known that DNA damage causes the supernumerary centrosomes by a mechanism in which centrosomes continue to duplicate during cell cycle arrest at checkpoints. We show here that ionizing radiation induces the overduplication of centrosomes in a dose-dependent manner, and that the level of overduplication is pronounced in BRCA1- and NBS1-deficient cells, even though their checkpoint control is abrogated. Conversely, marginal increases in overduplication were observed in Ku70- and DNA-PKcs-deficient cells, which are intact in checkpoint control. The frequency of radiation-induced overduplication of centrosomes might be associated with DNA repair, as it was decreased with reduced cell killing after protracted exposures to radiation. As a result, when the frequency of radiation-induced centrosome overduplication was plotted against radiation-induced cell killing, similar curves were seen for both protracted and acute exposures in wild-type cells, Ku70-deficient, and DNA-PKcs-deficient cells, indicating a common mechanism for centrosome overduplication. However, the absence of either BRCA1 or NBS1 enhanced radiation-induced overduplication frequencies by 2–4-fold on the basis of the same cell killing. These results suggest that radiation-induced centrosome overduplication is regulated by at least two mechanisms: a checkpoint-dependent pathway involved in wild-type cells, Ku70-deficient and DNA-PKcs-deficient cells; and a checkpoint-independent pathway as observed in BRCA1-deficient and NBS1-deficient cells. | |||||
| 書誌情報 |
Cancer Science 巻 101, 号 12, p. 2531-2537, 発行日 2010-12 |
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| ISSN | ||||||
| 収録物識別子タイプ | ISSN | |||||
| 収録物識別子 | 1347-9032 | |||||
