| Project/Area Number |
15K19004
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
General medical chemistry
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
Honda Shinya 東京医科歯科大学, 難治疾患研究所, 助教 (90532672)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2016: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | オートファジー / 赤血球 / がん / 中心体 |
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| Outline of Final Research Achievements |
Macroautophagy is a central mechanism in cellular metabolism by degrading parts of their cytoplasm and organelles using lysosomal enzymes. Previously, our group discovered the macroautophagy independent of Atg5 and Atg7, named Alternative autophagy. Recently, we reported alternative autophagy have an essential role for mitochondria clearance during erythrocyte differentiation.
This project aims to unravel the mechanisms of the alternative autophagy. To determine the essential molecule for the progression of alternative autophagy, we examine the proteome and microarray analysis using erythroid cells derived from wild type and alternative autophagy deficient mice. From these analysis, we identified the two candidate proteins, phospholipase and ubiquitin ligase. Contribution of both proteins to the alternative autophagy was determined by an analysis using MEF cells. In addition, we identified new function of conventional autophagy for the cell migration and regulation of centrosome number.
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