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2016 Fiscal Year Final Research Report

SAPKs and PLK4 maintain the numerical integrity of centrosomes

Research Project

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Project/Area Number 15K19003
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field General medical chemistry
Research InstitutionThe University of Tokyo

Principal Investigator

Nakamura Takanori  東京大学, 医科学研究所, 助教 (30707576)

Project Period (FY) 2015-04-01 – 2017-03-31
KeywordsMAPK / SAPK / PLK4 / 中心体 / 染色体不安定性
Outline of Final Research Achievements

Centrosomes function as bipolar spindles, which are essential for equal chromosome segregation. Therefore centrosome duplication is strictly regulated to once per cell cycle. Even under stress condition, centrosome number is maintained in normal cells. However, the molecular mechanism had remained unclear. We have reported that p53 and SAPK pathways cooperatively regulate PLK4-diriven centrosome duplication under stress, thereby maintaining the numeral integrity of centrosomes. This time we identified the novel target of SAPK in centrosome duplication arrest. Moreover we tried to elucidate the mechanism by which PLK4 translocalizes to mother centrioles.

Free Research Field

分子生物学、細胞生物学

URL: 

Published: 2018-03-22  

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