| Project/Area Number |
08457599
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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 |
Biological pharmacy
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| Research Institution | HOKKAIDO UNIVERSITY |
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Principal Investigator |
ARIGA Hiroyoshi Hokkaido Univ., Fac.of Pharm., Prof., 薬学部, 教授 (20143505)
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| Co-Investigator(Kenkyū-buntansha) |
ARIGA Sanae Hokkaido Univ., Coll.of Med.Tech., Prof., 医療技術短期大学部, 教授 (90184283)
TAKRA Takahiro.Y. Hokkaido Univ., Fac.of Pharm., Inst., 薬学部, 助手 (70197036)
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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 |
¥7,800,000 (Direct Cost: ¥7,800,000)
Fiscal Year 1997: ¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 1996: ¥4,200,000 (Direct Cost: ¥4,200,000)
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| Keywords | MYC / cell transformation / cell cycle / apoptosis / transcroption / DNA replication / c-myc / 転写因子 / cDNAクローニング / 癌遺伝子 |
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| Research Abstract |
We have identified several proteins that interact with C-MYC.These were classified to 4 group ; factor for DNA replication (MSSP), for transcription (AMY-1, MM-1. CBF), for cell-cycle control (p21), and for apoptosis induction (Pim-1). Of the proteins, MSSP futrher interacts with DNA polymerase alpha and PCNA directly, and cdk2 indirectly. C-MYC interacts with PCNA-binding region of p21 to rescue the inhibition of DNA replication by p21. A novel protein AMY-1 interacts the N-terrninal, so called transactivation domain of C-MYC,to stimulate transcriptional activity of C-MYC.AMY-1 was translocated from cytoplasm to nucleus after G1/S transition. Pim-1 is serine/threonine kinase and its target protein was identified, PAP-1. Pim-1 also phosphorylates CDC25 whose gene is known to be a transcriptional targer of C-MYC.These results suggest that a versatile functions of C-MYC occur by a distinguished protein complex during cell cycle.
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