2012 Fiscal Year Final Research Report
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 |
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Project Period (FY) |
2011 – 2012
|
Keywords | HTLV-1 |
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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