| Project/Area Number |
16590213
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General pharmacology
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| Research Institution | Fukuoka University |
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Principal Investigator |
IWAMOTO Takahiro Fukuoka University, School of Medicine, Lecturer, 医学部, 講師 (20300973)
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| Co-Investigator(Kenkyū-buntansha) |
MIGITA Keisuke Fukuoka University, School of Medicine, Assistant, 医学部, 助手 (10352262)
ARAI Yuji National Cardiovascular Center Research Institute, Department of Bioscience, Laboratory Chief, バイオサイエンス部, 室長 (30202724)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2005: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 2004: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | Na^+ / Ca^<2+> exchanger / Cation transporter / Expression system / Transgenic mice / Tissue distribution / イオントランスポーター / 薬理学 / 生理学 |
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| Research Abstract |
Abnormal intracellular Na^+ metabolism is related to several diseases, such as hypertension, arteriosclerosis, ischemic injury, renal failure, and diabetes. Recently, we found that the role of vascular Na^+/Ca^<2+> exchanger in the pathogenesis of salt-dependent hypertension using specific exchange inhibitors and genetically engineered mice. In this study, we searched a new Na^<+->driven cation transporter, which may be involved in Na^+-dependent diseases, and identified the new transporter by gene analyses using specific motif sequences (α-repeat) of Na^+/Ca^<2+> exchanger superfamily. The identified gene was partially homologous to K^+-dependent Na^+/Ca^<2+> exchanger (NCKX). This new NCKX was abundantly expressed in heart, smooth muscle, and skeletal muscle. When this new NCKX cDNA was expressed in mammalian cells, we could detect Na^+-dependent Ca^<2+> transport activity. We are currently preparing genetically engineered mice for this new NCKX. In near future, we would like to examine the functional and pathophysiological importance of this new Nat^+-driven cation transporter using genetically engineered mice.
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