Establish of mutant S19 ribosomal protein dimer functional deficient mice
| Project/Area Number |
22590362
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Experimental pathology
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| Research Institution | Kumamoto University |
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Principal Investigator |
NISHIURA Hiroshi 熊本大学, 大学院・生命科学研究部, 助教 (90284760)
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| Co-Investigator(Kenkyū-buntansha) |
ARAKI Kimi 熊本大学, 生命資源・研究支援センター, 准教授 (90211705)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2012: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2011: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2010: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | S19 リボソームタンパク質 / ダイアモンドブラックファン貧血症 / C5a 受容体 / モデルマウス / ケモタキシス / アポトーシス / S19リボソームタンパク質 / S19リボソーム蛋白質 / 貧血マウスモデル / ノックインマウス / ダイヤモンドブラックファン貧血症 |
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| Research Abstract |
In contrast to wild-type mice, numbers of bone marrow cells, spleen cells, and peripheralerythrocytes were slightly but significantly decreased in RP S19 oligomer functionaldeficient (Knock-In) mice. Moreover, a ratio of basophilic erythroblasts in Knock-In micewas also decreased based on the CD71/TER119 expression values in FACS analysis. When arecovering time of erythrocytes is measured in hemagglutinin-induced hemolytic anemiamice, the time was extended by Knock-In mice. Now, we start to examine whether RP S19oligomers are contributed with DBA. After that, we are to propose a maintenance systemof erythrocytes via RP S19 oligomer-dependent erythroblast island formation.
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Report
(4 results)
Research Products
(55 results)
