| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2020: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2019: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Outline of Final Research Achievements |
The purpose of this study was to clarify the role of cancer-related kinase AKT in chromosome instability and its regulatory mechanism. We found that in metaphase, AKT1 and AKT3 were localized to partially overlap Aurora kinase in the central spindle, and that treatment with AKT inhibitors multipolarized the tubulin spindle that acts on chromosome division. Furthermore, we found KIF23 as a new target molecule candidate for AKT. Phosphorylation of KIF23 by AKT was found to be involved in the localization of KIF23 to the midbody during cell division, demonstrating that AKT3 functions in the cell division mechanism.
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