| Project/Area Number |
62580111
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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 |
物質生物化学
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| Research Institution | Department of Biochemistry, Faculty of Medicine, University of Tokyo |
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Principal Investigator |
SANAI Yutaka Department of Biochemistry, Faculty of Medicine, University of Tokyo., 医学部(医), 助手 (40150289)
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| Project Period (FY) |
1987 – 1988
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| Project Status |
Completed (Fiscal Year 1988)
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| Budget Amount *help |
¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 1988: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 1987: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | Ganglioside / oncogene / シアル酸転移酵素 / 遺伝子クローニング / ヒトメラノーマ |
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| Research Abstract |
In order to elucidate the molecular mechanism on the expression of GD3 ganglioside associated with oncogenesis of cells, I examined the isolation of the genomic DNA controlling the expression of GD3 ganglioside which was well known as human melanoma associated antigen by employing cosmid shuttle vector and monoclonal antibody. Transfection of the cosmid library derived from human melanoma cells and repeated cell sortings of the fluorescence-bright population enabled to enrich the antigen positive transfectants. Six groups of indipendent clones were rescued from the GD3 positive transfectants by in vitro packaging procedure. However, these isolated clones lacked the capability of the induction of GD3 in the recipient L cells. These suggested the expression of GD3 in L cells were controlled by more than single gene. Nuclear type oncogenes such as adenovirus E1A and myc were also able to induce GD3 in rat 3Y1 cells, but other type oncogenes (src gene fammily and ras) could induce sialosylparagloboside altematively. These suggested expression of GD3 in transformed cells were related to the common function of the nuclear type oncogene.
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