Investigation of the molecular mechanism underlying Dok-3-mediated suppression of osteoclast fusion

2021 Fiscal Year Final Research Report

• Project/Area Number: 19K07362
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 48040:Medical biochemistry-related
• Research Institution: The University of Tokyo
• Principal Investigator: Inoue-Yamauchi Akane (井上茜) 東京大学, 医科学研究所, 助教 (90541970)
• Project Period (FY): 2019-04-01 – 2022-03-31
• Keywords: 破骨細胞

Outline of Final Research Achievements

Osteoclasts are responsible for bone resorption, which is essential for maintaining bone homeostasis. Efficient bone resorption requires differentiation and maturation of osteoclasts including cell-to-cell fusion; indeed, the absence of osteoclast fusion reduces bone-resorbing activity, leading to increased bone mass. In the present study, I investigated the mechanism underlying osteoclast fusion, focusing on adaptor protein Dok-3.

Free Research Field

骨代謝学

Academic Significance and Societal Importance of the Research Achievements

本研究の成果は、これまでに報告のない破骨細胞の融合を担うシグナル伝達の解明に取り組むことで、破骨細胞融合制御の新たなメカニズムを理解するための手がかりを得た点、また、これまでにない視点での破骨細胞融合を標的とする骨代謝性疾患治療法開発へ向けた基礎的な知見を得た点において意義深い。