| 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)
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| 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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