| Project/Area Number |
60560093
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
応用生物化学・栄養化学
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| Research Institution | Kyoto University |
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Principal Investigator |
KITO Makoto Research Institute for Food Science, 食糧科学研究所, 教授 (60027183)
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| Co-Investigator(Kenkyū-buntansha) |
URADE Reiko Research Institute for Food Science, 食糧科学研究所, 教務職員 (90167289)
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| Project Period (FY) |
1985 – 1986
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| Project Status |
Completed (Fiscal Year 1986)
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| Budget Amount *help |
¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1986: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1985: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | Unsaturated fatty acid mutant of animal cells in culture / Chinese hamster V79-UF / Phospholipid molecular species / Arachidonic acid / リン脂質分子種 |
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| Research Abstract |
V79-UF cells were isolated from Chinese hamster V79 cells as a cell line that requires exogenous unsaturated fatty acid for growth. The reduced formation of monoenoic fatty acids in V79-UF was due to deficiency in the stimulation of stearoyl-CoA desaturase which is a key enzyme to convert saturated fatty acids to monoenoic fatty acids. V79-UF cells incorporated arachidonic into phospholipids. Polyunsaturated phospholipid molecular species thus formed were distributed in a higher amount in the intracellular membrane than in plasma membrane. Plasma membrane fluidity was not controlled by the phosphatidylcholine/phosphatidylethanolamine ratio, but by accumulation of cholesterol. Hence, it is postulated that the loss of cholesterol in the endoplasmic reticulum by the one-way direction of cholesterol transport from the endoplasmic reticulum to plasma membrane makes fluidity of the endoplasmic reticulum abnormal. Such change may cause the cells lethal.
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