| Project/Area Number |
08457369
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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 |
Cerebral neurosurgery
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| Research Institution | Kumamoto University |
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Principal Investigator |
SAYA Hideyuki Kumamoto University School of Medicine, Professor, 医学部, 教授 (80264282)
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| Project Period (FY) |
1996 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥7,200,000 (Direct Cost: ¥7,200,000)
Fiscal Year 1997: ¥2,900,000 (Direct Cost: ¥2,900,000)
Fiscal Year 1996: ¥4,300,000 (Direct Cost: ¥4,300,000)
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| Keywords | glioma / apoptosis / p53 gene / bcl-2 gene / NDP kinase / Bcl-2遺伝子 / 発現クローニング / EBNA-1 / アデノウイルス |
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| Research Abstract |
It has been known that p53 protein plays an important role in not only cell cycle regulation but also apoptosis. In the present study, we attempted to elucidate molecular mechanisms which negatively regulate p53-induced apoptotic signal. During the period of April, 1991 through March, 1992, we identified the following findings :
1)To investigate the effects of the expression of Bcl-2 protein in cancer cells on the apoptosis induced by adenoviral-medicated p53 gene transfer, we transfected the bcl-2 gene into KoTCC-1 cell that does not express the Bcl-2 protein. The Bcl-2-transfected cells exhibited significantly higher resistance to p53-induced apoptosis than did either the parental cell or the vector-only transfected cell both in vitro and in vivo.
2)A Hela cDNA library constructed in an episomal plasmid was introduced into EBNA-1 stable expression cells for complementation of the adenoviral p53-induced apoptosis. The cDNA insert of the plasmid which was recovered from the apoptosis-resistant cells encoded a 194 amino acid polypeptide that has significant homology with E.coli nucleoside diphoshate kinase (NDPK). The NDPK is known to catalyze a transfer of the terminal phosphate of triphosphate nucleosides to diphosphate nucleosides by a ping-pong mechanism which regulates balance of nucleoside pool, that may inhibit apoptosis induced by p53 expression.
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