Autophagic neurodegeneration in molecular pathogenesis of chorea-accanthocytosis
| Project/Area Number |
23390291
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Psychiatric science
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| Research Institution | Kagoshima University |
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Principal Investigator |
SANO Akira 鹿児島大学, 医歯(薬)学総合研究科, 教授 (30178800)
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| Co-Investigator(Kenkyū-buntansha) |
NAKAMURA Masayuki 鹿児島大学, 大学院・歯学総合研究科, 准教授 (90332832)
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| Project Period (FY) |
2011-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥19,370,000 (Direct Cost: ¥14,900,000、Indirect Cost: ¥4,470,000)
Fiscal Year 2013: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2012: ¥7,410,000 (Direct Cost: ¥5,700,000、Indirect Cost: ¥1,710,000)
Fiscal Year 2011: ¥8,970,000 (Direct Cost: ¥6,900,000、Indirect Cost: ¥2,070,000)
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| Keywords | 有棘赤血球舞踏病 / chorein / オートファジー / α-tubulin / 脱アセチル化 / 微小管 / VPS13A / 免疫沈降 / 免疫細胞化学 / HEK293細胞 / 結合タンパク質 / 結合蛋白質 / 免疫組織化学 / マクロオートファジー / ミトファジー |
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| Research Abstract |
Co-immunopreticipation assay using extracts from chorein-overexpressing cells showed that chorein, the protein responsible for chorea-acanthocytosis (ChAc), co-precipitated with alpha-tubulin and HDAC6, probably leading to facilitation of alpha-tubulin deacetylation. Cell viability assay revealed that cells stably expressing chorein, significantly preserved cell viability during nutrient deprivation. These results suggest that chorein interacts with the cytoskeletal proteins and may play an important role in autophagic process, including in the protection against starvation-induced cell damages. Disruption of this cell protection mechanism may involved in molecular pathogenesis of ChAc.
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Report
(4 results)
Research Products
(28 results)
