Molecular mechanisms that maintain centrosome integrity by SAPK and mechanisms that regulate PLK4 localization to centrosomes.
| Project/Area Number |
25893039
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
General medical chemistry
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| Research Institution | The University of Tokyo |
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Principal Investigator |
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| Project Period (FY) |
2013-08-30 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | SAPK / PLK4 / p38 / JNK / 中心体 / p53 / 染色体安定性 / シグナル伝達 / ストレス応答 |
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| Outline of Final Research Achievements |
Centrosomes function as bipolar mitotic spindles, which are essential to chromosomal equal segregation. Centrosome biogenesis is control by PLK4 and centrosome duplication is tightly regulated to once per cell cycle in normal cells. In contrast, centrosome number is often increased after various stresses in cancer cells. The molecular mechanisms underlying centrosome overduplication process, however, had remained obscure. Recently we reported that the two major stress responsive SAPK pathway and p53 pathway cooperatively PLK4 kinase activity and PLK4-driven centrosome duplication under stress. Moreover, we identify the novel substrate of SAPK in centrosome duplication arrest.
We also identify several proteins, which regulate PLK4 localization to centrosomes.
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Report
(3 results)
Research Products
(8 results)
