| Project/Area Number |
15K15082
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Pathological medical chemistry
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| Research Institution | Hiroshima University |
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Principal Investigator |
MATSUURA SHINYA 広島大学, 原爆放射線医科学研究所, 教授 (90274133)
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| Co-Investigator(Kenkyū-buntansha) |
宮本 達雄 広島大学, 原爆放射線医科学研究所, 講師 (40452627)
柳原 啓見 広島大学, 原爆放射線医科学研究所, 助教 (50719474)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2016: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2015: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
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| Keywords | 細胞老化 / モデル生物 / モデル動物 |
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| Outline of Final Research Achievements |
Germline mutations that reduce BubR1 induce premature ageing phenotypes in mice. However, the molecular mechanism underlying the premature ageing phenotypes remain incompletely understood. The aim of this study is to study whether ageing phenotypes are associated with instability of telomeres. We generated the human mutation (1833delT) knock-in mice. During this process, we obtained a mouse carrying a 12-bp deletion (Δ608-611 LAST) in exon 15 of BubR1. No homozygous mice for 1833delT were generated, suggesting that complete BubR1 deficiency causes the embryonic lethality. On the other hand, compound heterozygotes for 1833delT and the 12-bp deletion were generated according to the Mendelian inheritance. However, accelerated aging was not observed in these mice before the age of 5 months.
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