| Project/Area Number |
15K08398
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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 |
Experimental pathology
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| Research Institution | Nagoya University |
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Principal Investigator |
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| Project Period (FY) |
2015-10-21 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | 鉄代謝 / DMT1 / DMT1 Associated Protein / 細胞増殖 |
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| Outline of Final Research Achievements |
Transport of iron is carried by divalent metal transporter 1(DMT1) in mammalian cell. In this grant, K562 was employed as an erythroid precursor model to study DMT1 Associated Protein(DAP). An analysis of DAP amino acid sequence revealed the binding domain to PBR. Protoporpyrin IX(PPIX) is presumed to bind with PBR, suggesting the interaction between DAP and PPIX via PBR. The expression levels of DAP, DMT1, transferrin receptor 1(TfR1), ferritin heavy chain(FTH) were examined after exposure of PPIX. PPIX decreased the protein level of DAP and DMT1 at 1 h. mRNA level of DAP was induced at 8 h and protein level was recovered at 24 h, while, mRNA of DMT1 was not increased until 24 h after PPIX exposure. C/EBPa, which transcribe DMT1 mRNA, were decreased by PPIX treatment. PPIX-induced degradation of DAP, FTH, DMT1 was presumed to be carried in lysosome and proteasome. The combination of lysosomal and proteasomal inhibitor were most effective way to prevent the degradation of FTH.
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