| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2010: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2009: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2008: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Research Abstract |
Cellular senescence is an irreversible growth arrest and is presumed to be a natural barrier to tumor development. Like telomere shortening, certain defects in chromosome integrity can trigger senescence. Kinetochores are multi-protein complexes formed on a specialized region of each chromosome, designated the centromere. Kinetochore function is essential for the faithful segregation of chromosomes during mitosis and meiosis. I have demonstrated that primary cells appear to induce cellular senescence in response to fatal kinetochore dysfunction in circumstances under which some of key centromere proteins and/or the spindle assembly checkpoint (SAC) proteins are not functioning properly. These observations suggest that, like telomeres, kinetochores may also play a crucial role in regulating commitment to the senescent state.
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