2004 Fiscal Year Final Research Report Summary
Roles of APGubiquitylation-like modification during differentiation and maintenance of neuronal cells.
| Project/Area Number |
15590254
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General medical chemistry
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| Research Institution | JUNTENDO UNIVERSITY |
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Principal Investigator |
ISEI Tanida JUNTENDO UNIVERSITY, SCHOOL OF MEDICINE, DEPARTMENT OF BIOCHEMISTRY, ASSISTANT PROFESSOR, 医学部, 講師 (30296868)
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| Project Period (FY) |
2003 – 2004
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| Keywords | AUTOPHAGY / UBIQUITYLATION-LIKE / ATG / APG gene / MAP-LC3 / GABARAP / GATE-16 / 3rd Cell Death / DIFFERENTIATION TO NEURON |
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| Research Abstract |
ATG-ubiquitylation-like modification is essential for autophagy in yeast, plant, and mammals. ATG7 is a key enzyme essential for the reaction. We generated a conditional knock-out mouse of ATG7 Mouse liver lacking Atg7 resulted in a severe hepatomegaly with inflammation, leading to a loss of viability under starvation. During generating the conditional mouse, we showed that human Atg4B is an unique cysteine protease for carboxyl cleavage of LC, GABARAP, and GATE-16, and is delipidating enzyme for LC3-and GABARAP-phospholipid conjugate. Furthermore, we showed that human LC3 is an authentic modifier mediated by human Atg7 and Atg3. We also found a novel Ufml Ubl-modification system in mammals. In addition, we investigated several aspects of ATG-conjugation systems; Strauctural analysis of LC3 by NMR, Role of Rab7 in autophagy, and tissue-distribution of modified forms of LC3, GABARAP, and GATE-16. Now, we are generating a brain-specific ATG7-knockout mouse that will be a definitive tool for analyses of relations between autophagy and neurodegenerative diseases
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Research Products
(20 results)
