Elucidation of the role of alternative autophagy in hemophagocytotic syndrome
| Project/Area Number |
24689020
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| Research Category |
Grant-in-Aid for Young Scientists (A)
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| Allocation Type | Partial Multi-year Fund |
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| Research Field |
Human pathology
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
ARAKAWA Satoko 東京医科歯科大学, 難治疾患研究所, 助教 (90415159)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥27,040,000 (Direct Cost: ¥20,800,000、Indirect Cost: ¥6,240,000)
Fiscal Year 2013: ¥12,740,000 (Direct Cost: ¥9,800,000、Indirect Cost: ¥2,940,000)
Fiscal Year 2012: ¥14,300,000 (Direct Cost: ¥11,000,000、Indirect Cost: ¥3,300,000)
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| Keywords | オートファジー / マイトファジー / 赤血球 / 血球分化 / ミトコンドリア / 血球貪食症候群 |
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| Research Abstract |
Macroautophagy degrades subcellular constituents and some evidences indicate that it is involved in elimination of some organelles. In erythrocyte differentiation, mitochondria are removed from reticulocytes and it has been suggested that macroautophagy is required for it. Although it is believed that Atg5 and Atg7 are indispensable for macroautophagy, their role in this process is controversial. Recently, we discovered that mammalian cells possess Atg5/Atg7-independent macroautophagy as well as Atg5/Atg7-dependent macroautophagy and Ulk1 regulates the former process. We hypothesized that Ulk1-mediated Atg5/Atg7-independent macroautophagy is involved in the elimination of mitochondria from reticulocytes. In this study, we demonstrated the removal of mitochondria in Ulk1-deficient erythrocytes was impaired. Furthermore, Ulk-1 deficient embryo becomes anemia. This would be attributed to the more susceptibility of the erythrocytes to the apoptosis and the engulfment by macrophage.
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Report
(3 results)
Research Products
(24 results)
