Does dephosphorylation of DNA-damage repair protein XRCC4 trigger enhancement of apoptosis?
Project/Area Number |
26740020
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Risk sciences of radiation and chemicals
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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
|
Project Status |
Completed (Fiscal Year 2016)
|
Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
|
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.
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Report
(4 results)
Research Products
(5 results)