| Project/Area Number |
12470490
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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., Grad. School of Pharm., Prof., 大学院・薬学研究科, 教授 (20143505)
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| Co-Investigator(Kenkyū-buntansha) |
KITAURA Hirotake Hokkaido Univ., Grad. School of Pharm., Inst., 大学院・薬学研究科, 助手 (10281817)
TAIRA Takahiro Hokkaido Univ., Grad. School of Pharm., Asso. Prof., 大学院・薬学研究科, 助教授 (70197036)
ARIGA Sanae Hokkaido Univ., Coll. Med. Tec., Prof., 医療技術短期大学部, 教授 (90184283)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥10,400,000 (Direct Cost: ¥10,400,000)
Fiscal Year 2001: ¥4,700,000 (Direct Cost: ¥4,700,000)
Fiscal Year 2000: ¥5,700,000 (Direct Cost: ¥5,700,000)
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| Keywords | c-Myc / oncogene / tumor suppressor / transformation / transcription factor / co-repressor / embryonic lethal / spermatogenesis / c-myc / co-repressor / 転写制御 / 細胞周期 / タンパク質分解 / リン酸化 / クロマチン |
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| Research Abstract |
1).MM-1
MM-1 was found to have an mutation of alanine (A) at amino acid number 157 to arginine (R) in a high frequency of the patients of leukemia, lymphoma and scc-type of tongue cancers. This mutation of MM-1 abrogates all the functions of MM-1 to c-Myc, including repression of activities for transcription, cell transformation, and cell growth. The transrepression pathway of MM-1 to c-Myc was found to be carried out by the recruitment of HDAC complex by TIF1b that MM-1 binds. Furthermore, we have found that MM-1 also stimulates the degradation of c-Myc in a ubiquitin-independent manner and that this activity of A157R mutation of MM-1 was hampered. We also identified the splicing isoforms of MM-1 by an alternative splicing of the gene mapped to chromosome 12 and each isoform was found to be distinctly located in cells.
2).AMY-1
AMY-1 was found to bind to WAVE1 to relocalize the site for actin polymerization and also to AKAP84, an anchoring protein of A-kinase, for participating in the spermatogenesis.
3). MSSP
Disruption of mssp gene in mice showed some embryonic lethality, indication that MSSP functions in early embryogenesis.
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