| Project/Area Number |
21710057
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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 |
Risk sciences of radiation/Chemicals
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| Research Institution | Kyoto University |
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Principal Investigator |
TOMIDA Junya Kyoto University, 放射線生物研究センター, 研究員 (50511367)
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| Research Collaborator |
ITAYA Akiko , 日本学術振興会特別研究員 (50535812)
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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 |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2010: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2009: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | ファンコニ貧血 / FANCI / FANCD2 / 脱リン酸化酵素 / DNA損傷応答 / Fanconi貧血 / リン酸化 / DNA修復 / Fanconi貧 |
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| Research Abstract |
We have recently found out that novel Fanconi anemia (FA) protein FANCI is phosphorylated and functions as a switch to trigger FANCD2 monoubiquitination upon DNA damage or replication stress. FANCI itself is also monoubiquitinated, and we found that FANCI is de-phosphorylated immediately after the monoubiquitination. Thus, FANCI phosphorylation and de-phosphorylation must be important events in regulating the FA pathway. In this study, we wished to identify which phosphatase is involved in the regulation of FANCI phosphorylation levels. We tested every phosphatase genes encoded in the genome targeting phospho-serine or threonine using siRNA, and found at least several of them are involved in FA pathway activation. Further study will be needed to clarify how these phosphatases functions in the FA pathway.
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