Analysis of PKX-deficient mice that indicate placental disorder.

2019 Fiscal Year Final Research Report

• Project/Area Number: 17K11213
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Obstetrics and gynecology
• Research Institution: Kobe 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
• 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.

Free Research Field

実験動物学、生殖生理学

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。