| Budget Amount *help |
¥27,560,000 (Direct Cost: ¥21,200,000、Indirect Cost: ¥6,360,000)
Fiscal Year 2014: ¥6,890,000 (Direct Cost: ¥5,300,000、Indirect Cost: ¥1,590,000)
Fiscal Year 2013: ¥8,970,000 (Direct Cost: ¥6,900,000、Indirect Cost: ¥2,070,000)
Fiscal Year 2012: ¥11,700,000 (Direct Cost: ¥9,000,000、Indirect Cost: ¥2,700,000)
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| Outline of Final Research Achievements |
Ionizing irradiation and ultraviolets could alter genetic information by damaging genomic DNA. The damaged DNA should be detected and then repaired. For accurate and quick restoration of DNA information, DNA damage detection system and repair system must cooperate, however the underlying mechanism of that is still largely unknown. In this study, we focus on one of the checkpoint protein Rad9, and analyzed in order to understand the positive and negative feedback system that regulate Rad9 behavior from activation to inactivation, by phosphorylation. First, we constructed the in vitro reconstitution system to investigate the interaction between Rad9 complex and its loader complex to DNA damage site, Rad17 complex. The ATP dependent interaction is observed and suggested that ATP dependent conformational change govern the regulation. Furthermore we identified Plk1 as a negative regulator that phsphorylate human Rad9 orthologue.
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