Does dephosphorylation of DNA-damage repair protein XRCC4 trigger enhancement of apoptosis?

2016 Fiscal Year Final Research Report

• Project/Area Number: 26740020
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Risk sciences of radiation and chemicals
• Research Institution: Kanazawa Medical University
• Principal Investigator: SUNATANI Yumi 金沢医科大学, 医学部, 助教 (70581057)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: アポトーシス / リン酸化

Outline of Final Research Achievements

A role of DNA-damage repair protein XRCC4 in apoptosis is not well understood. I have revealed that XRCC4 enhances apoptosis after its cleavage by caspases, and this enhancing effect requires the phosphorylation of XRCC4Thr233. I have further shown that the cleaved fragment of XRCC4 is dephosphorylated during apoptosis. In this study, I asked whether the dephosphorylation of phosphorylated XRCC4Thr233 enhances apoptosis. The results showed that the dephosphorylation of XRCC4Thr233 leads to apoptosis enhancement. Furthermore, protein kinase DNA-PK and/or CK2 are/is involved in the phosphorylation, whereas protein phosphatase PP2A is involved in the dephosphorylation of XRCC4Thr233.

Free Research Field

細胞生物学