molecular analysis of Prader-Willi syndrome model mice with imprinting mutation
| Project/Area Number |
25461555
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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 |
Pediatrics
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| Research Institution | Nagasaki University |
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Principal Investigator |
KISHINO Tatsuya 長崎大学, 先導生命科学研究支援センター, 准教授 (70315232)
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| Project Period (FY) |
2013-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
Fiscal Year 2013: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
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| Keywords | プラダーウィリー症候群 / インプリンティング / モデルマウス / DNAメチル化 / トランスジェニックマウス / Necdin / Mkrn3 / necdin / Magel2 / Snord116 / G9a阻害剤 / ゲノムインプリンティング / magel2 / mkrn3 / BACトランスジェニックマウス / Snrpn |
|---|
| Outline of Final Research Achievements |
We created Prader-Willi syndrome (PWS) model mice, which show neonatal lethality because of abnormal DNA methylation on the PWS imprinting center (IC). We analyzed molecular mechanism of establishment of genomic imprinting in gametes and early embryos using our PWS model mice. We found that the main epigenetic factor which could affect gene expression in the imprinted region is genomic constitution and next DNA methylation after implantation. To recue neonatal lethality in PWS model mice, we created Ndn and Mkrn3 transgenic mice, but both of them could not rescue the PWS model mice.
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Report
(5 results)
Research Products
(10 results)
