Molecular physiology of labor induction via placental protein kinase Nrk

2014 Fiscal Year Final Research Report

• Project/Area Number: 25650031
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Functional biochemistry
• Research Institution: Tokyo Institute of Technology
• Principal Investigator: DENDA Kimitoshi 東京工業大学, 生命理工学研究科, 助教 (50212064)
• Co-Investigator(Renkei-kenkyūsha): KOMADA Masayuki 東京工業大学, 大学院大学院生命理工学研究科, 教授 (10225568)
• Project Period (FY): 2013-04-01 – 2015-03-31
• Keywords: Ser/Thrキナーゼ / 胎盤 / 妊娠 / 分娩不全 / 遺伝子ノックアウト

Outline of Final Research Achievements

Nrk (Nik-related kinase) encoded in the X chromosome is a physiologically mysterious Ser/Thr protein kinase, which belongs to the germinal center kinase family. On a whole-body level in mice, disruption of the nrk gene resulted in the placental overgrowth, suggesting that Nrk acts as a regulator of cell proliferation in the organ. It has also observed that the nrk-null fetuses influence the pregnant dam to be delay of labor.
To shed light on the molecular mechanisms lying behind the nrk-null phenotyes, we isolated a series of Nrk-binding proteins by using two-hybrid analysis and co-immunoprecipitation. In addition, proteomics analysis against the nrk gene distrupted placenta were performed using the high performance two-dimentional polyacrylamide gel electrophoresis. We identified several proteins whose expression levels were varied significantly. Our research how Nrk acts as a device for controlling labor induction will clarify the complexities in the process of pregnancy and labor.

Free Research Field

生化学・細胞生物学・分子生理学