2014 Fiscal Year Final Research Report
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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| Keywords | SAPK / PLK4 / p38 / JNK / 中心体 / p53 / 染色体安定性 |
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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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| Free Research Field |
分子生物学
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