| Project/Area Number |
14370748
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Biological pharmacy
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| Research Institution | Kumamoto University |
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Principal Investigator |
KAI Hirofumi Kumamoto University, Molecular Medicine, Professor, 大学院・医学薬学研究部, 教授 (30194658)
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| Co-Investigator(Kenkyū-buntansha) |
IKEMIZU Shinji Kumamoto University, Structural Biology, Associate Professor, 大学院・医学薬学研究部, 助教授 (60333522)
ARIMA Hidetoshi Kumamoto University, Pharmaceutical Sciences, Associate Professor, 大学院・医学薬学研究部, 助教授 (50260964)
YAMADA Gen Kumamoto University, Developmental Biology, Professor, 生命資源研究・支援センター, 教授 (80174712)
SHUTO Tsuyoshi Kumamoto University, Molecular Medicine, Research Associate, 大学院・医学薬学研究部, 助手 (80333524)
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| Project Period (FY) |
2002 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥13,700,000 (Direct Cost: ¥13,700,000)
Fiscal Year 2004: ¥3,900,000 (Direct Cost: ¥3,900,000)
Fiscal Year 2003: ¥4,300,000 (Direct Cost: ¥4,300,000)
Fiscal Year 2002: ¥5,500,000 (Direct Cost: ¥5,500,000)
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| Keywords | CFTR / molecular chaperone / calnexin / calreticulin / MEF / lysozyme / PML nuclear body / ETS transcription factor / ガン / Heat Shock Protein / 分子シャペロン / vitamin K / heat shock protein |
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| Research Abstract |
1.CFTR was exported from the ER to cis-Golgi and early endosome, suggesting that CFTR transport in the early secretory pathway may utilize a non-conventional pathway. This CFTR trafficking pathway may be a target for pharmacological modulation that selectively stimulates CFTR transport.
2.Curcumin may have an unique effect as an accelerator of CFTR trafficking by decreasing calreticulin, a negative regulator of CFTR and have important implications in developing therapeutic approaches that target the trafficking of CFTR.
3.The recruitment of MEF to PML nuclear bodies regulates lysozyme transcription in epithelial cells.
4.MEF may play an important role in regulating HBD2 expression in epithelial cells.
5.MEF is a tumor suppressor gene on the X chromosome with activities that are opposite to those of ETS-2.
6.PML stimulated MEF transcriptional activity, resulting in the up-regulation of endogenous HBD 2 expression.
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