| Project/Area Number |
02807027
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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 |
General medical chemistry
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| Research Institution | Osaka University |
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Principal Investigator |
OKAMOTO Kazuki Biomedical Research Center Osaka University Medical School Assistant professor, 医学部, 助手 (40177085)
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| Project Period (FY) |
1990 – 1992
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| Project Status |
Completed (Fiscal Year 1992)
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| Budget Amount *help |
¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 1992: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 1991: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 1990: ¥900,000 (Direct Cost: ¥900,000)
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| Keywords | glucocorticoid / receptor / translocation promoter / ホルモン・レスポンス・エレメント |
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| Research Abstract |
1. We have found and purified an ATP-stimulted factor that enhances the nuclear binding of "activated" glucocorticoidreceptor complex (GRC) in the presence of ATP. ASTP has a molecular weight of 49K (SDS-PAGE) and works a dimer in native form. ASTP binds to histone and is thought to be involved in nuclear acceptor sites of GRC. Using anti-ASTP antibody, I identified and sequenced cDNA encoding ASTP from rat liver cDNA library. It has 2.4 Kbp sequence with open reading frame of 1.5 Kbp. The predicted protein has 524 amino acids and contains 8 peptide sequences derived from purified ASTP treated with lysineendopeptidase and V8 protease. Now, I am trying to constract an ASTP expression vector.
2. To clarify the physiological significance of the interaction of ASTP with GRC, I investigated the existance of ASTP and GRC in glucocorticoid-resistant tumor cells. Using anti-ASTP and anti-GRC antibodies, I found that the glucocorticoid-resistant tumor cells have GRC indistinguishable from that of normal rat liver, however, the tumor cells have no ASTP protein. These results indicate that ASTP is an important factor in gene transcription by glucocorticoid hormone.
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