Study on TRIC and MG23 channels

2020 Fiscal Year Final Research Report

• Project/Area Number: 18H02597
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Single-year Grants
• Section: 一般
• Review Section: Basic Section 48020:Physiology-related
• Research Institution: Kyoto University
• Principal Investigator: Takeshima Hiroshi 京都大学, 薬学研究科, 教授 (70212024)
• Project Period (FY): 2018-04-01 – 2021-03-31
• Keywords: 小胞体 / Ca2+ストア / Ca2+シグナリング

Outline of Final Research Achievements

In our analyzing TRIC and MG23 proteins in intracellular Ca2+ stores, we detected several new findings including major issues as described below. 1) TRIC-A-mediated activation of ryanodine receptors is essential for normal cardiac functions, and this activation is likely caused by direct protein-protein interaction between them. 2) In contrast to TRIC-A, TRIC-B frequently shows cooperative gating, and the unique may contribute to the support of IP3 receptor-mediated Ca2+ release. 3) We found spontaneous Ca2+ entry mediated by TRP family channel members in growth plate chondrocytes and peritoneal macrophages.

Free Research Field

細胞生理学

Academic Significance and Societal Importance of the Research Achievements

細胞内Ca2+シグナルは多様な機能を制御するため、その分子機序の解を目指す本研究のは学術的意義は高い。また、本研究により明らかになったCa2+シグナルを構築する分子機序は、新たな創薬標的を提供し、医薬領域への波及効果を有する。