Mechanism of PDZ domain protein regulation for HTLV-1 tumorigenesis
| Project/Area Number |
23590537
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Virology
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| Research Institution | Niigata University |
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Principal Investigator |
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | HTLV-1 / ATL / PDZ / ROS / MAGI-1 / Tax / PDZドメイン / 白血病 / シグナル伝達 / 成人T細胞白血病 |
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| Research Abstract |
HTLV-1 is a causative agent of adult T-cell leukemia. HTLV-1 encoded protein Tax1 interacts with various PDZ domain containing proteins, leading to their dysfunction and transformation of infected T cells. We identified MAGI-1 as a new Tax1 interacting PDZ domain containing protein. MAGI-1 expression was dramatically reduced in Tax1 transformed T cells and HTLV-1 infected T cells. Knockdown of MAGI-1 increased intracellular ROS. Conversely, overexpression of MAGI-1 reduced intracellular ROS. These results suggest that MAGI-1 is a regulator of ROS production and MAGI-1 inactivation by Tax1 and subsequent aberrant ROS production is involved in Tax1 mediated tumorigenesis.
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Report
(4 results)
Research Products
(24 results)
