| Project/Area Number |
22790298
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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 | Kyoto University (2012-2013)
Kyoto Prefectural University of Medicine (2010-2011) |
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Principal Investigator |
YOKOTA Asumi 京都大学, 医学(系)研究科(研究院), 研究員 (00571556)
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| Project Period (FY) |
2010-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2012: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2011: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2010: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
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| Keywords | Runx1 / 翻訳後修飾 / 転写因子 / 造血 |
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| Research Abstract |
There are nine serine/threonine residues in the C-terminal region of mouse Runx1, which are capable of being phosphorylated. We have made two Runx1 mutants; Dephospho-mimetic 1-9A and phospho-mimetic 1-9D mutant, of which all of these serine/threonine residues were mutated to alanine or aspartic acid, respectively. In luciferase assay, transcriptional activities of these mutants were affected compared with WT Runx1. However, protein expression levels or intracellular localizations were not changed.
Next we have established Runx1 mutant-KI ES cells. 1-9A or 1-9D mutant has been knocked-in to Runx1-KO ES cells. Both 1-9A and 1-9D KI ES cells could differentiate toward hematopoietic cells, indicating that these mutants retain their activity, which could rescue the differentiation blockade of Runx1 KO ES cells. As the frequencies of hematopoietic colonies were affected by these mutations, it is suggested that phosphorylation status of Runx1 might regulate its biological activity.
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