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Analysis of PKX-deficient mice that indicate placental disorder.

Research Project

Project/Area Number 17K11213
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Obstetrics and gynecology
Research InstitutionKobe University (2019)
Hokkaido University (2017-2018)

Principal Investigator

MORIOKA YUKA  神戸大学, 医学研究科, 准教授 (00360264)

Project Period (FY) 2017-04-01 – 2020-03-31
Project Status Completed (Fiscal Year 2019)
Budget Amount *help
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2019: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2018: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Keywords胎盤異常 / 周産期障害 / プロテインキナーゼ
Outline of Final Research Achievements

In this study, we confirmed that PKX deficiency resulted in activation of AKT in differentiated trophoblast stem cells (day6-TSC). AKT is known to be comprised three highly homologous isoforms: AKT1, AKT2, and AKT3. All three AKT isoforms were expressed in day6-TSC with almost equivalent levels between wild-type and PKX-null genotypes. However, upregulation of phosphorylation was observed in all three AKT isoforms derived from PKX-null cells compared with wild-type cells. Because PKX deficiency did not influence expression and the activity of the factors which have been already known as a regulation factor of AKT, it was suggested that PKX regulate AKT phosphorylation through unknown mechanism.

Academic Significance and Societal Importance of the Research Achievements

AKTのリン酸化メカニズムについては盛んに研究されており、これまでに多くの制御因子が報告されているが、PKXは含まれていない。本研究により、PKXはAKTリン酸化の制御に関与するものの、既知の経路を介していないことが示された。これは、AKTリン酸化に新たな経路が存在する可能性を示唆する結果であり、学術的に高い意義を有する。

Report

(4 results)
  • 2019 Annual Research Report   Final Research Report ( PDF )
  • 2018 Research-status Report
  • 2017 Research-status Report

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Published: 2017-04-28   Modified: 2021-02-19  

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