| Project/Area Number |
21791262
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
General surgery
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| Research Institution | St.Marianna University School of Medicine |
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Principal Investigator |
HAYAMI Ryosuke St.Marianna University School of Medicine, 医学部, 助教 (00529894)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2010: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2009: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 乳癌 / BRCA1 / BACH1 / BRIP1 / ノックアウトマウス / ノックインマウス / BACH1/BRIP1 |
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| Research Abstract |
In order to analyze BACH1 role in DNA damage repair through its interaction with BRCA1, we generated BACH1 null and BACH1^<S990A/S990A> ES cell. In addition, we generated BACH1 knock-out mice and BACH1^<S990A/S990A> knock-in mice in order to analyze the phenotype of these.
BACH1 null cells showed the fearfully DNA repair defect following DNA damage. BACH1 WT cells certainly showed the few DNA repair defect following DNA damage. And furthermore, BACH1^<S990A/S990A> cells showed more defective than BACH1 WT cells, but they showed less defective than BACH1 null cells in DNA repair following DNA damage.
AS for the phenotype, BACH1 knock-out mice and BACH1^<S990A/S990A> knock-in mice developed different types of tumors. Furthermore, BACH1 knock-out mice are hypersensitive to DNA damage.
Therefore, the role of BACH1, as well as the interaction of BACH1 and BRCA1 proved biologically to be very important for DNA repair and checkpoint mechanism following DNA damage.
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