| Project/Area Number |
07557161
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| Research Category |
Grant-in-Aid for Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Section | 展開研究 |
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| Research Field |
Biological pharmacy
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| Research Institution | Teikyo University |
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Principal Investigator |
TAKANO Tatsuya Teikyo Univ., Fac.of Pharm.Sci., Professor, 薬学部, 教授 (40124995)
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| Co-Investigator(Kenkyū-buntansha) |
EYA Seiji Teikyo Univ., Fac.of Pharm.Sci., Research Associate, 薬学部, 助手 (20221814)
MORI Masahiro Teikyo Univ., Fac.of Pharm.Sci., Research Associate, 薬学部, 助手 (00230079)
ITABE Hiroyuki Teikyo Univ., Fac.of Pharm.Sci., Assistant Professor, 薬学部, 講師 (30203079)
IMANAKA Tsuneo Teikyo Univ., Fac.of Pharm.Sci., Associate Professor, 薬学部, 助教授 (50119559)
SATO Ryuichiro Osaka Univ., Fac.of Pharm.Sci., Associate Professor, 薬学部, 助教授 (50187259)
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| Project Period (FY) |
1995 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥15,100,000 (Direct Cost: ¥15,100,000)
Fiscal Year 1997: ¥4,200,000 (Direct Cost: ¥4,200,000)
Fiscal Year 1996: ¥4,600,000 (Direct Cost: ¥4,600,000)
Fiscal Year 1995: ¥6,300,000 (Direct Cost: ¥6,300,000)
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| Keywords | Cholesterol / LDL Receptor / SREBP / Transcription / Atherosclerosis / HMGCoA合成酵素 / 高脂血症 / SRE / 転写調節 / ALLN / LDL受容体転写因子 / HMGCoA還元酵素 / コレステロール合成 |
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| Research Abstract |
Animal cells synthesize cholesterol from acetyl CoA through a series of more than 20 enzymatic reactions. In addition, cells obtain cholesterol from plasma in the form of lowdensity lipoprotein (LDL), which is internalized via the LDL receptor and hydrolyzed to free cholesterol in lysosomes. Each cell must balance these internal and external sources while avoiding sterol shortage or over-accunrulation. Both the biosynthetic and uptake pathways are well-regulated through feedback control. When cells are cultured in the presence of LDL,the activity of both 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) synthase and HMG CoA reductase decline by more than 90% and the number of LDL receptors also decreases. In the absence of LDL,the cells maintain high activities of these two enzymes, which are rate-limiting enzymes of the biosynthetic pathway, and also maintain a large number of LDL receptors on their surface. We assess recent progress in understanding the mechanisms involved in transcriptional and posttranscriptional regulation of intracellular cholesterol metabolism.
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