| Project/Area Number |
25840076
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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 |
Cell biology
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| Research Institution | Osaka University |
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Principal Investigator |
SHIBUTANI Shusaku 大阪大学, 医学(系)研究科(研究院), 助教 (20534473)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | オートファジー / Atg |
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| Outline of Final Research Achievements |
It has been known that damage to endosomes or lysosomes induces autophagy, and this autophagy induction appears to be related to the isolation/elimination of invasive bacteria and damaged lysosomes. The ULK1 complex, a protein complex that functions at early stages of autophagy, is known to be recruited to damaged endosomes/lysosomes, suggesting that the recruitment plays a role in the autophagy induction around damaged endosomes/lysosomes. In this study, we focused on FIP200, a subunit of the ULK1 complex, and identified the regions of FIP200 that are responsible for its recruitment to damaged endosomes and for its interaction with ULK1, respectively. We further analyzed the functions of these regions in autophagy induction.
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