Autophagy regulation by HIV-1 Vpr
Project/Area Number |
25460573
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Virology
|
Research Institution | Kinki University |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
MIYAZAWA Masaaki 近畿大学, 医学部, 教授 (60167757)
|
Project Period (FY) |
2013-04-01 – 2016-03-31
|
Project Status |
Completed (Fiscal Year 2015)
|
Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
|
Keywords | ウイルス / HIV / オートファジー / HIV-1 / Vpr |
Outline of Final Research Achievements |
We had discovered that HIV-1 Vpr has the ability to control an autophagy. Here we have tried to identify cellular factor(s) involved in this regulation and disclose its molecular mechanisms. We found that the Vpr-mediated autophagy regulation does not depend on cellular factors which have previously been reported to interact with Vpr. Interestingly, Vpr has two functions in autophagy regulation, augmentation of autophagosome formation and inhibition of autolysosome maturation. We identified a key factor by which Vpr facilitates autophagosome formation. Vpr seems to activate the cellular protein binding to the identified factor to initiate autophagy. We find that Vpr does not disturb the autolysosome formation but clearly impairs the acidity of cellular acidic compartments. These results indicate that Vpr decrease enzymatic function in acidic organelles through disruption of pH, leading to inhibition of autolysosome function.
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Report
(4 results)
Research Products
(6 results)