Identification of the p63-associated proteins regulating the pathological mechanisms of ectodermal dysplasia

2022 Fiscal Year Final Research Report

• Project/Area Number: 20K07364
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 49010:Pathological biochemistry-related
• Research Institution: Kobe Gakuin University
• Principal Investigator: Suzuki Daisuke 神戸学院大学, 栄養学部, 講師 (10439698)
• Project Period (FY): 2020-04-01 – 2023-03-31
• Keywords: TP63 (Trp63) / 外胚葉異形成症候群 / 幹細胞 / 上皮細胞 / 増殖 / リン酸化 / 分化

Outline of Final Research Achievements

Loss of normal functional of the transcription factor p63 is known to lead a congenital disorder, ectodermal dysplasia. However, the molecular mechanisms controlling p63 function remain unclear. To find the molecular machinery to regulate p63 function, we here screened p63-associated proteins through proteome analysis and then identified a candidate protein which is associated with p63 protein C-terminus. This protein showed that a kinase activity to phosphorylate p63 molecule in vitro. Furthermore, downregulation of the kinase gene expression in epithelial stem cells degraded the performance of colony formation and impaired their proliferative potential of the stem cells.

Free Research Field

幹細胞学、分子生物学、細胞生物学

Academic Significance and Societal Importance of the Research Achievements

本研究で得られた成果は、幹細胞のcell cycleを調節する技術開発に繋がる点で大きな意義をもち、上記疾患の根治的治療法の開発をはじめ、幹細胞による組織修復を促す再生医療、そして老化組織の新陳代謝を促す抗加齢医療の技術発展につながることが期待される。