The pathogenic mechanism of HTLV-1 leukemogenesis via novel binding protein of Tax1
Project/Area Number |
23790498
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Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Multi-year Fund |
Research Field |
Virology
|
Research Institution | Niigata University |
Principal Investigator |
|
Project Period (FY) |
2011 – 2012
|
Project Status |
Completed (Fiscal Year 2012)
|
Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
|
Keywords | HTLV-1 / Tax1 / USP10 / ストレス顆粒 / 活性酸素種 / ROS / G3BP1 |
Research Abstract |
We examined functional roles of USP10 and its binding partner G3BP1. We found that G3BP1 elevates the steady-state ROS level by inhibiting the antioxidant activity of USP10. However, following exposure to arsenic, G3BP1 and USP10 induce the formation of stress granules, which uncovers the antioxidant activity of USP10. We also found that the antioxidant activity of USP10 requires the protein kinase activity of ATM.
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Report
(3 results)
Research Products
(8 results)