| Project/Area Number |
06454591
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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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., Sci. Prof., 薬学部, 教授 (20143505)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥7,100,000 (Direct Cost: ¥7,100,000)
Fiscal Year 1995: ¥2,900,000 (Direct Cost: ¥2,900,000)
Fiscal Year 1994: ¥4,200,000 (Direct Cost: ¥4,200,000)
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| Keywords | C-MYC / DNA BINDING / TRANSCRIPTION FACTOR / APOPTOSIS / TRANSFORMATION / CELL CYCLE / N-myc / DNA複製 / 転写調節 / トランスフォーメーション / hsp70 / MHC classI |
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| Research Abstract |
C-MYC is making complex with a variety of proteins to play numerous roles. We have identified and cloned cDNAs encoding MYC-binding proteins.
1) MSSP MSSP was found as an DNA binding protein on origin/enhancer in c-myc gene. MSSP plays a role as DNA replication and transcription factor. MSSP binds to N-terminal portion of C-MYC via its C-terminus portion.
2) AMY-1 Using two hybrid system we cloned a novel cDNA encoding AMY-1. AMY-1 was located in the nucleus, and bound to N-terminal region of C-MYC via its C-terminus. AMY-1 acted as a transcription factor and stimulated transcriptional activity of C-MYC.AMY-1 also stimulated C-MYC's transforming activity dramatically.
3) Pim-1 Pim-1 was known to transform cells with c-myc. Here we found that Pim-1 was directly associated with C-MYC.Pim-1 induced apoptosis by its overexpression. Signal transduction from Pim-1 to C-MYC may contribute apoptosis pathway.
4) DNA polymerase a and cdk2 C-MYC and MSSP were also bound to N-terminal portion of catalytic subunit of DNA polymerase a and cdk2, a protein for G1/S checkpoint protein. MSSP stimulated polymerase activity. These results indicated that MSSP/C-MYC play a key role G1/S,especially the initiation of DNA replication.
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