| Project/Area Number |
23590332
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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 |
General medical chemistry
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| Research Institution | Osaka University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
NAKAGAWA Yoshiaki 京都大学, 農学研究科, 准教授 (80155689)
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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 |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2012: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2011: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
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| Keywords | myocardin / MRTF-A/B / Crm1 / importin α/β1 / CCG-1423 / 核移行 / 核外移行 / 上皮間葉転換 / 細胞内局在制御 / thymosinβ4 / Arp5 / SRF / 平滑筋細胞 |
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| Research Abstract |
Myocardin (Mycd), a key factor for the smooth muscle cell differentiation, is constitutively located in the nucleus, whereas myocardin-related transcription factors A and B (MRTF-A/B), mostly reside in the cytoplasm and translocate to the nucleus in response to a signaling-induced decrease in G-actin. MRTF-A/B play a critical role in induction of epithelial-mesenchymal transition (EMT). Here, we investigated the regulatory mechanism for subcellular localization of Mycd family members and their related cell functions. Our studies revealed the following findings. 1) Regulatory mechanism of Crm1-mediated nuclear export of Mycd family members: critical differences in the regulation between Mycd and MRTF-A/B. 2) Inhibitory mechanism of CCG-1423 (a novel inhibitor of EMT) for the nuclear import of MRTF-A/B. 3) Activation of MRTF-A nuclear import by thymosin beta 4. 4) Novel function of Mycd RPEL motifs: actinrelated protein 5-mediated inhibition of Mycd function.
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