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“Complex DNA double strand break” preferably activates DNA end resection for homologous recombination repair
https://repo.qst.go.jp/records/64487
https://repo.qst.go.jp/records/64487831fc29a-a9f4-4414-b04d-29809ae3472f
| Item type | 会議発表用資料 / Presentation(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 2012-01-30 | |||||
| タイトル | ||||||
| タイトル | “Complex DNA double strand break” preferably activates DNA end resection for homologous recombination repair | |||||
| 言語 | ||||||
| 言語 | jpn | |||||
| 資源タイプ | ||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_c94f | |||||
| 資源タイプ | conference object | |||||
| 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 |
矢島, 浩彦
× 矢島, 浩彦× 中島, 菜花子× 平川, 博一× 岡安, 隆一× 藤森, 亮× 矢島 浩彦× 中島 菜花子× 平川 博一× 岡安 隆一× 藤森 亮 |
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| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | DNA double strand break (DSB) induced by ionizing radiation (IR) is a deleterious damage for cell survival and genome integrity. It is repaired by two major pathways, non-homologous end-joining (NHEJ) and homologous recombination (HR). It has been shown that NHEJ is dominant throughout the cell cycle after X- or gamma-ray exposure to human cells. Meanwhile, it is thought that heavy-ion radiation (e.g., carbon-ion, iron-ion) gives rise to clustered DNA damages consisting of not only strand breaks but also aberrant bases in the vicinity of DSB (called “complex DSB”), and our previous work suggested that the efficiency of NHEJ is diminished for repair of “complex DSB” induced by heavy-ion radiation. There seems difficulty in the process of NHEJ to repair “complex DSB” and consequently the role of HR may be expanded in the response to heavy-ion radiation. To elucidate heavy ion-induced DNA damage response, we analyzed U2OS cells irradiated with X-ray and heavy-ion radiation, and found that CtIP was intensely phosphorylated after heavy-ion irradiation especially at early time point. This suggests that the “complex DSB” effectively evokes DNA end resection activity for the HR, in which CtIP has a critical role. This notion was supported by an observation that RPA2 phosphorylation level, a good indicator of end resection, was also much elevated following the CtIP phosphorylation. In addition, results of our preliminary experiments suggested that HR deficient cells are hypersensitive to heavy-ion radiation. Taken together, the homologous recombination pathway would be a good target for radio-sensitization particularly in heavy-ion therapy. |
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| 会議概要（会議名, 開催地, 会期, 主催者等） | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | 第34回日本分子生物学会年会 | |||||
| 発表年月日 | ||||||
| 日付 | 2011-12-16 | |||||
| 日付タイプ | Issued | |||||
