| Project/Area Number |
07670162
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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 |
Pathological medical chemistry
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| Research Institution | Hokkaido University |
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Principal Investigator |
NISHIHIRA Jun Central Research institute Hokkaido University School of Medicine, Lecturer, 医学部, 講師 (30189302)
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| Co-Investigator(Kenkyū-buntansha) |
TANAKA Isao Graduate School of Science, Hokkaido University, Professor, 理学部, 教授 (70093052)
INOUE Yoshiro Department of Anatomy, Hokkaido University School of Medicine, Professor, 医学部, 教授 (20051584)
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1996: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1995: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | glutathione / macrophage / endotoxin schock / macrophage migration inhibitory factor / マクロファージ遊走阻止因子 / 内毒素 |
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| Research Abstract |
Macrophage migration inhibitory factor (MIF) was the first lymphokine discovered in lectin-activated T lymphocytes. It was originally identified by its ability to prevent the migration of macrophages out of a capillary tube in vitro. Human MIF cDNA was first cloned from T-lymphocytes, which revealed that the protein consists of 114 amino acid residues. MIF has long been considered to be expressed exclusively in activated T-lymphocytes ; however, a recent report indicated that macrophages are another major source of MIF.Various novel biological properties of MIF have been discovered. MIF is the major secretory protein released by anterior pituitary cells in response to lipopolysaccharide stimulation and is considered to play a central role in endotoxemia. During the course of our MIF study, we cloned rat MIF cDNA,and reported its physicochemical properties. We moreover succeeded in the crystallization of both human and rat MIFs, and elucidated the tertiary structure of rat MIF at 2.2 * resolution. Furthermore, we identified the expression of MIF in human skin and cornea, which indicated that expression of MIF was not limited to T lymphocytes and macrophages.
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