Calcium-signaling abnormality of polyglutamine diseases
| Project/Area Number |
26461315
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Neurology
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| Research Institution | Yokohama City University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
田中 章景 横浜市立大学, 医学研究科, 教授 (30378012)
多田 美紀子 横浜市立大学, 附属病院, 助教 (30722467)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | ポリグルタミン病 / カルシウムシグナリング / カルシウムチャネル |
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| Outline of Final Research Achievements |
We examined association of polyglutamine disease and the calcium-signaling abnormality. Polyglutamine diseases are chronic, progressive neurodegenerative diseases caused by expansion of a glutamine tract in widely expressed genes and a heterogeneous group of dominantly inherited neurodegenerative disorders affecting the cerebellum and its associated pathways. These cause proteins are associated with cell death by calcium-signaling abnormality. We determined the possibility that a CACNA1A calcium channel in the polyglutamine disease was associated with abnormal cause protein formation of polyglutamine disease and identified a calcium channel subtype binding to cause protein. We confirmed the distribution of the calcium channel subtype expressions showed possibility reflecting a lesion of each polyglutamine disease and showed resistibility and vulnerability for the neurodegeneration.
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Report
(4 results)
Research Products
(1 results)
