Increasing DSB ends mobility with 53BP1 improve Non homologous end joining
| Project/Area Number |
23510067
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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 | Kanazawa Medical University |
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Principal Investigator |
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| Project Period (FY) |
2011-04-28 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,590,000 (Direct Cost: ¥4,300,000、Indirect Cost: ¥1,290,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 53BP1 / Rad18 / TRF2 / DNA二重鎖切断 / テロメア / T-SCE / 染色体末端結合修復 / CO-FISH / T-SCE(テロメア末端姉妹染色体分体組換) / DNA二重鎖切断端 / 非相同末端結合修復 / テロメア末端姉妹染色体分体組換 / 末端結合修復 / 非保護テロメア末端 |
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| Outline of Final Research Achievements |
53BP1 plays a key role in repair for DNA double strand breaks. 53BP1 binds ends of DSBs and facilitates rejoining of both ends. I and co-authors reported that (1) 53BP1 plays a role in a novel pathway distinct from the Ku-dependent and Artemis-dependent NHEJ (Non homologus end joining) pathways (Genes Cells, 11: 935, 2006). (2) RAD18 interacts with 53BP1 and is recruited to DSB sites in a 53BP1-dependent manner specifically during G1-phase. RAD18 monoubiquitinates 53BP1, consequently, enhances retention of 53BP1 at DSBs site (Nucleic Acids Res., 37: 2176, 2009). Depletion of TRF2 (one of shelterin components) arises dysfunctional and unprotected telomeres. Telomere deprotection activate ATM dependent DNA repair pathway and promote NHEJ. DNA repair proteins including 53BP1 recognize unprotected telomeres as DSBs. I investigated that the interaction between 53BP1 and Rad18 works in the rejoing of telomere ends.
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Report
(5 results)
Research Products
(11 results)
