The epigenetic mechanism of synaptic molecules in autism
| Project/Area Number |
21790974
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Pediatrics
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| Research Institution | University of Yamanashi |
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Principal Investigator |
HIRASAWA Takae University of Yamanashi, 大学院・医学工学研究部, 助教 (10402083)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2010: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2009: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 脳 / エピジェネティクス / 自閉症 / 神経科学 / 脳・神経 / 発現制御 |
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| Research Abstract |
Rett syndrome, one of the childhood autism, is identified MeCP2 as responsible protein. We assumed the dysregulation of genes involved in synapse formation of symptom in this syndrome. We identified MALS-1 gene is a new gene regulated by MeCP2. In the cerebral cortex of MeCP2-KO mice, MALS-1 protein expression was decreased compared to wild type. Neuro2A, a neuroblastoma cells, the siRNA-MeCP2 also showed the decrease of expression of MALS-1 mRNA. MeCP2 is a DNA methylation of genes that contribute to MALS-1, unlike previous reports it was suggested that MeCP2 is enhanced by this protein expression. Therefore, the symptom of autism in Rett syndrome is suggested that the MALS-1 related to the abnormal expression of synapse formation by a decline.
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Report
(3 results)
Research Products
(19 results)
