| Project/Area Number |
17019027
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| Research Category |
Grant-in-Aid for Scientific Research on Priority Areas
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| Allocation Type | Single-year Grants |
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| Review Section |
Biological Sciences
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| Research Institution | Hamamatsu University School of Medicine |
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Principal Investigator |
MINOSHIMA Shinsei Hamamatsu University School of Medicine, 光量子医学研究センター, 教授 (90181966)
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| Co-Investigator(Kenkyū-buntansha) |
OHISHI Kentaro 浜松医科大学, 光量子医学研究センター, 助教 (80345826)
OHTSUBO Masafumi 浜松医科大学, 光量子医学研究センター, 助教 (10327653)
HOTTA Yoshihiro 浜松医科大学, 医学部, 教授 (90173608)
森脇 真一 大阪医科大学, 医学部, 准教授 (40303565)
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| Co-Investigator(Renkei-kenkyūsha) |
MORIWAKI Shinichi 大阪医科大学, 医学部, 教授 (40303565)
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| Research Collaborator |
中西 伸夫
細野 克博
王 春霞
ISMAIL Thanseem
杉山 将隆.
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| Project Period (FY) |
2005 – 2009
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| Project Status |
Completed (Fiscal Year 2009)
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| Budget Amount *help |
¥66,100,000 (Direct Cost: ¥66,100,000)
Fiscal Year 2009: ¥12,700,000 (Direct Cost: ¥12,700,000)
Fiscal Year 2008: ¥12,700,000 (Direct Cost: ¥12,700,000)
Fiscal Year 2007: ¥13,500,000 (Direct Cost: ¥13,500,000)
Fiscal Year 2006: ¥13,600,000 (Direct Cost: ¥13,600,000)
Fiscal Year 2005: ¥13,600,000 (Direct Cost: ¥13,600,000)
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| Keywords | ゲノム悉皆解析法 / 拡張侯補遺伝子アプローチ / データベース / 光関連疾患 / 遺伝性眼疾患 / 緑内障 / 加齢黄斑変性 / 遺伝学 / 遺伝子 / ゲノム / 情報工学 / 脳神経疾患 / 原因遺伝子 / 遺伝子変異 / モデル動物 / 拡張候補遺伝子アプローチ |
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| Research Abstract |
Using various techniques based on genomic analysis, we approached the onset mechanism of glaucoma and age-related macular degeneration (AMD) which lead the cause of blindness in Japan. For glaucoma, we newly isolated the proteins which interact with either of myocilin or optineurin. From the known functions of those interacting proteins, involvement of novel phenomenon and cellular function in the development of glaucoma was suggested. For AMD, a rat experimental model of retinal photic injury was employed. Since the susceptibility in the retinal photic injury by irradiation of visible light depended on the rat strain, we performed a genetic analysis to identify the responsible genes. Two loci on rat chromosome 5 and 19 were necessary for the 'susceptible' trait. Cloning of these 2 responsible genes is ongoing to analyze the possible association of their human counterparts on the onset of AMD will be done.
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