| Project/Area Number |
12470051
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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 |
Experimental pathology
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| Research Institution | HOKKAIDO UNIVERSITY |
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Principal Investigator |
MORIUCHI Tetsuya Hokkaido Univ. Institute For Genetic Medicine, Prof., 遺伝子病制御研究所, 教授 (20174394)
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| Co-Investigator(Kenkyū-buntansha) |
HAMADA Jun-ichi Hokkaido Univ. institute For Genetic Medicine, Asso. Prof., 遺伝子病制御研究所, 助教授 (50192703)
TADA Mitsuhiro Hokkaido Univ. Institute For Genetic Medicine, Asso. Prof., 遺伝子病制御研究所, 助教授 (10241316)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥10,000,000 (Direct Cost: ¥10,000,000)
Fiscal Year 2001: ¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2000: ¥6,500,000 (Direct Cost: ¥6,500,000)
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| Keywords | LEC rat / NF-kB / transcription / p53 / glutathione peroxidase / LEC / 肝臓 / GPx1 |
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| Research Abstract |
The long-Evans Cinnamon (LEC) rat is a mutant strain that develops hereditary hepatitis and spontaneous hepatocellular carcinoma. Using immortalized hepatocyte cell lines, 93C13 (LEC hepatocyte) and 93A16 (control LEA hepatocyte), we searched for a trans-acting factor lacking in the LEC rat liver. Based on our previous finding that glutathione peroxidase (GPx1) expression was consistently reduced in the LEC rat liver, we selected GPx1 gene for its analysis. Transient transfection assays of the constructs containing 5'-flanking sequences fused to the luciferase gene showed that 93C13 cells lacked factor(s) cooperating with p53 and NF-kB. These results suggested that decreased expression of GPx1 in LEC rat hepatocytes is notdue to lack of specific transcription factor but to abnormality in basic transcription factor complex.
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