Molecular function of NBS1 in non-homologous end joining and mechanisms of chromosome instability.
| Project/Area Number |
24510070
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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 |
Risk sciences of radiation/Chemicals
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| Research Institution | Kyoto University |
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Principal Investigator |
KATO Akihiro 京都大学, 放射線生物研究センター, 研究員 (70423051)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,720,000 (Direct Cost: ¥4,400,000、Indirect Cost: ¥1,320,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2012: ¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
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| Keywords | DNA修復 / DNA二重鎖切断 / 放射線 / NBS1 / ナイミーヘン症候群 |
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| Outline of Final Research Achievements |
Nijmegen breakage syndrome (NBS) is a member of chromosome instability syndromes. The responsible gene product of NBS, NBS1, quickly responds to DNA double strand breaks (DSBs) induced by ionizing radiation, and functions to prevent chromosome instability, carcinogenesis and cell death. However, molecular mechanisms of these functions remain largely unknown. In this study, we proved that NBS1 functions in non-homologous end joining (NHEJ), which is one of the major pathways of DSB repair. In addition, we also revealed that the specific region of NBS1 has a specialized function in NHEJ.
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Report
(4 results)
Research Products
(10 results)
