Selection of DSBs repair pathways in heat-induced cell death mediated by BRCA2
| Project/Area Number |
26463052
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Surgical dentistry
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| Research Institution | Nara Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
高橋 昭久 群馬大学, 重粒子線医学推進機構, 教授 (60275336)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 温熱 / 相同組み換え修復 / DNA二本鎖切断 / BRCA2 / ＢＲＣＡ２ / ＤＮＡ二本鎖切断 |
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| Outline of Final Research Achievements |
We showed that heat-induced DSBs are repaired by HR pathways. If phosphorylation of Ku was important for heat-induced DSBs, these phosphorylated enzyme (ATR etc.) inhibitors could block phosphorylation and disassociation from DSBs of Ku. In the colony forming assays, combination use with ATR inhibitor (VE-821) and heat was more sensitive than heat only. In human tongue squamous cell carcinoma cells, immunocytochemical staining for γH2AX following heat showed that the expression in combination use with VE-821 and heat was about twice as much as heat only. This results suggest that phosphorylation of Ku might be important for heat-induced DSBs
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Report
(4 results)
Research Products
(2 results)
