| Project/Area Number |
22790281
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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 |
General medical chemistry
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| Research Institution | Mie University |
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Principal Investigator |
SUGIMURA Kazuto 三重大学, 大学院・医学系研究科, 助教 (90452226)
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| Project Period (FY) |
2010 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2011: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2010: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | Erk2 / NCFC症候群 / p53 / 血球・血管内皮 / 細胞老化 / Noonan症候群 |
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| Research Abstract |
Hematopoietic and endothelial cell lineage-specific gain of function mutation of Erk2 in mice resulted in lower rate of birth, lower body weight, and lower body length. The mice had NCFC syndrome-like physical characteristics such as unique facial abnormalities, indicating that constitutive activation of Erk2 was the cause for the part of pathological features in NCFC syndrome. Moreover, p53 was likely to be involved in the phenotype, suggesting that p53-targeted treatment might be effective to the NCFC syndrome-linked pathologies.
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