| Project/Area Number |
04670559
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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 |
Circulatory organs internal medicine
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| Research Institution | Jikei University School of Medicine |
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Principal Investigator |
KATO Mitsutoshi Internal Medicine, Aoto Hospital, Jikei University School of Medicine. Lecturer., 医学部・内科講師 (60177475)
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| Co-Investigator(Kenkyū-buntansha) |
NAGAI Makoto Internal Medicine, Aoto Hospital, Jikei University School of Medicine. Research, 医学部, 研究助手
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| Project Period (FY) |
1992 – 1993
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| Project Status |
Completed (Fiscal Year 1993)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1993: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1992: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | ADP / ATP carrier protein / cardiomyopathic hamster / mitochondria / ATP carrier protein / Cardiomyopathy / J‐2‐N cardiomyopathic hamster |
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| Research Abstract |
The ADP/ATP carrier protein(AAC), located in the mitochondrial inner membrane, plays an important role in the mitochondrial energy metabolism. ATP is transported from matrix to cytoplasm by AAC and at the same time ADP is transported inversely. Cloning was performed using myocardium from Bio14.6 hamsters, J-2-N cardiomyopathic hamsters bred in our laboratory, and Golden hamster. The AAC contest was significantly decreased in J-2-N hamsters as compared with Golden hamsters. cDNA of AAC was cloned from cDNA library of the human fibroblast by PCR.The human cDNA was then used to screen Golden hamster AAC cDNA, which was used as a probe in the latter steps. Genomic DNA was prepared from cardiac muscle of the each strain hamster and DNA libraries were constructed. From these libraries, we have succeeded in obtaining genomic DNA of cardiac AAC in hamster. Also RNA dot blot hybridization analysis was performed. The highest mRNA level for AAC was observed in Golden hamster followed by J-2-N with high serum CK, J-2-N with lower serum CK and Bio14.6. These results suggest that decreased mRNA levels of AAC is one of the mechanisms which explain the abnormalities of cardiac metabolism in J-2-N cardiomyopathic hamsters.
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