Analysis of TCR signaling dependent mDia activation molecular mechanism

2016 Fiscal Year Final Research Report

• Project/Area Number: 15K18986
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: General pharmacology
• Research Institution: Kyoto University
• Principal Investigator: Thumkeo Dean 京都大学, 医学研究科, 特定准教授 (40372594)
• Project Period (FY): 2015-04-01 – 2017-03-31
• Keywords: T細胞 / mDia / TCRシグナル / アクチン

Outline of Final Research Achievements

T cell is essential for adaptive immunity. T cells is activated by TCR signaling that is indispensable for T cell development and function. I have previously reported that mDia facilitates TCR signaling through the regulation of actin polymerization by utilizing mDia 1/3 double deficient mice. In this study, I further unraveled the molecular mechanism of mDia activation in TCR signaling. We found that mDia is activated by the small G protein RhoA upon TCR stimulation. In addition, using T cells expressing EGFP-mDia3, I found that mDia is localized at the cell periphery in T cells upon TCR stimulation. Therefore, mDia is activated upon TCR stimulation through RhoA at the cell periphery and facilitate TCR signaling through its actin polymerization activity.

Free Research Field

薬理学