| Project/Area Number |
13670155
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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 |
Pathological medical chemistry
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| Research Institution | The Tokyo Metropolitan Institute of Medical Science |
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Principal Investigator |
SUZUKI Toshiaki The Tokyo Metropolitan Institute of Medical Science, Dept. of Molecular Oncology, Researcher, 東京都臨床医学総合研究所, 主任研究員 (90252171)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2002: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 2001: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | ubiquitin / parkinsonism / protein degradation / パーキンソン病 / ユビキチンリガーゼ / プロテアソーム / パーキン / 品質管理 / CHIP / 分子シャペロン / 線虫 |
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| Research Abstract |
Parkin belongs to a family of proteins with conserved UBL and RING finger motifs. Mutations in parkin cause the autosomal recessive juvenile form of parkinsonism (AR-JP). In the patients with parkin mutations, there is selective loss of dopaminergic neurons without the presence of Lewy bodies. Before this research, we showed that parkin had an ubiquitin protein-ligase activity. According to this, we began to identify the substrate and regulator of parkin. To this end, we performed yeast two-hybrid screening using parkin as a bait, purification of parkin binding proteins. Until now, we isolated some candidate of parkin substrate, and examining their reliability using C. elegans, which possesses possible parkin gene. We already isolated two allele of parkin mutant. Now we are analyzing the phenotype caused by disruption of parkin gene, although the parkin gene seems to be non-essential for the viability.
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