2013 Fiscal Year Final Research Report
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 |
Section | 一般 |
Research Field |
Virology
|
Research Institution | Niigata University |
Principal Investigator |
|
Project Period (FY) |
2011 – 2013
|
Keywords | HTLV-1 / ATL / PDZ / ROS / MAGI-1 / Tax |
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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Research Products
(13 results)