| Project/Area Number |
23591400
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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 |
Hematology
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| Research Institution | Fukushima Medical University |
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Principal Investigator |
SHIKAMA Yayoi 福島県立医科大学, 医学部, 准教授 (40291562)
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| Co-Investigator(Kenkyū-buntansha) |
SHICHISHIMA Tsutomu 福島県立医科大学, 医学部, 博士研究員 (10192105)
NOJI Hideyoshi 福島県立医科大学, 医学部, 講師 (20347214)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2013: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2011: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
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| Keywords | 骨髄異形成症候群 / FOS / 好中球 / RNA安定生 / 翻訳停止 / RNA 安定性 / mRNA安定性 / immediate early gene / HuR |
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| Research Abstract |
FOS is an immediate early gene whose expression level is rapidly increased under translation arrest in the cells exposed to DNA-damaging stresses. We found that translation arrest-induced elevation of FOS mRNA was attenuated in neutrophils from myelodysplastic syndrome (MDS) patients. The aberrant FOS mRNA induction was not due to reduced transcriptional activity but insufficient mRNA stabilization. In some patients, the expression levels of HuR, an mRNA-binding protein that stabilizes FOS mRNA, was decreased compared to those in healthy controls. Further, two microRNAs targeting FOS mRNA were increased in two-third of the patients tested. Our study indicated that the aberrant expressions of HuR and microRNAs resulted in the attenuated FOS mRNA induction in MDS.
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