| Project/Area Number |
15570152
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Molecular biology
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| Research Institution | National Cancer Center Research Institute |
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Principal Investigator |
OHTA Tsutomu National Cancer Center Research Institute, Genetic-Division, Section-Head, 腫瘍ゲノム解析情報研究部, 室長 (10290892)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 2004: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2003: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | NBS1 / Mre11 / DNA Chip / 電離放射線 / 抗がん剤 / 乳児白血病 / RAD50 |
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| Research Abstract |
It was known that when double strand DNAs were broken, p53 and Nbs1 in the Mre11/Rad50/Nbs1 protein complex were phosphorated by ATM. A lot of studies of p53 pathway were done. However, Nbs1 pathway is unclear. Then, I tried to analyze the Nbs1 pathway.
First, I made stable cell lines in which Nbs1 is expressed in NBS1 deficient cell. The NBS1 deficient cell was sensitive to γ-ray. The Nbs1 expressed cell was not sensitive to γ-ray, suggesting that Nbs1 participates in DNA repair pathway of double Strand DNA broken.
Using DNA chip, 1 analyzed gene expression profiling of NBS1 deficient cell. I have found a lot of genes which are regulated by Nbs1 in γ-ray treatment Next, I will analyze functions of these genes.
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