Analyses of WIPI family as a PI(3,5)P2 effector
| Project/Area Number |
15K18505
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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 |
Functional biochemistry
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| Research Institution | Fukushima Medical University |
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Principal Investigator |
Tamura Naoki 福島県立医科大学, 医学部, 助教 (70745992)
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| Research Collaborator |
Zhang Hong
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2017: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | オートファジー / 高浸透圧ストレス / WIPI / Ulk複合体 / autophagy / osmotic stress / TOR / リソソーム / エンドソ―ム / 浸透圧ストレス / イノシトールリン脂質 |
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| Outline of Final Research Achievements |
In this study, I focused on functions of WIPI family as a PI(3,5)P2-binding effector. First, I analyzed the subcellular localization of WIPI family under various conditions that the amount of PI(3,5)P2 was changed. As a result, WIPI-1 and WIPI-2 displayed punctate structures when cells were exposed to hyperosmotic stresses. Under hyperosmotic stresses, WIPI-1 and WIPI-2 were co-localized with autophagosomes and p62, a substrate of selective autophagy, was transported to lysosomes for degradation. Taken together, I concluded that an autophagic pathway is induced in response to hyperosmotic stresses. Unexpectedly, WIPI-1 and WIPI-2 functioned as a PI(3)P, a precursor of PI(3,5)P2, effector, but not as a PI(3,5)P2 effector. Interestingly, this autophagy did not require the Ulk complex in contrast to starvation-induced autophagy.
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Report
(4 results)
Research Products
(7 results)
