| Project/Area Number |
07670365
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Immunology
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| Research Institution | Chiba University, School of Medicine |
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Principal Investigator |
KANNO Masamoto School of Medicine, Chiba University ; Assoc.Prof., 医学部, 助教授 (40161393)
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1996: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1995: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | cell cycle / signal transduction / antigen receptor / Polycomb group gene / ポリコム遺伝子 / B細胞分化 / 細胞増殖 / c-myc / サイクリン |
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| Research Abstract |
mel-18 is a mammalian homologue of the Drosophila Polycomb group (PcG) gene encoding a sequence-specific transcriptional repressor. We found that the overexpression of mel-18 causes the cell cycle arrest of B-cells after stimulation of the BCR.Molecular analysis revealed that the downregulation of cyclin D2, cyclin E,CDK4, CDK6, CDK7, and CDC25A causes the impaired activities of cyclin-dependent kinases, resulting in hypophosphorylation of the Rb protein. We also demonstrated that c-myc is a direct target of Mel-18 and is downregulated upon mel-18 overexpression. c-Myc is known to regulate positively the expression of cdc25a and cyclin E.Thus we conclude that mel-18 negatively regulates the cell cycle progression through a new cascade starting from mel-18 to c-myc then cdc25a or cyclin E.
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