| Project/Area Number |
14571592
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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 |
Obstetrics and gynecology
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| Research Institution | Osaka Medical College |
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Principal Investigator |
OTSUKI Yoshinori Osaka Medical College, Faculty of Medicine, Professor, 医学部, 教授 (50140166)
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| Co-Investigator(Kenkyū-buntansha) |
UEKI Muinoru Osaka Medical College, Faculty of Medicine, Professor, 医学部, 教授 (40084892)
ITO Yuko Osaka Medical College, Faculty of Medicine, Assistant Professor, 医学部, 講師 (40148432)
LI Zhonglian Osaka Medical College, Faculty of Medicine, Research Associate, 医学部, 助手 (80319532)
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| Project Period (FY) |
2002 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2004: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2003: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2002: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | endometrium / bcl-2 / transcription / Biacore / c-Jun / Sp-1 / ERa / apoptosis / 子宮内膜 / 転写因子 / AP-1 / e-Jun / c-Fos / ATF-1 |
|---|
| Research Abstract |
The estrogen-estrogen receptor (ER) signalling pathway plays crucial physiologic roles not only in control of reproduction, but also the generation of cancer in breast and uterus. While some ER target genes have been identified containing the estrogen responsive element (ERE), others are activated eventually by estrogen via protein-protein interaction without binding to ERE. In a previous study we found out that the proliferative stage-specific expression of the bcl-2 gene in the glandular cells could be regulated by binding of c-Jun to its motifs in the promoter. Results from the present studies indicate that the menstrual cyclic expression of bcl-2 could be controlled by either the direct binding of ERa to ERE in the c-jun promoter or the interaction with c-Jun that binds to its motifs in the bcl-2 gene. Intriguingly, the transcriptionally active form of c-Jun phosphorylated at Ser73 was identified binding to the identified motifs in a menstrual cycle non-specific manner. Our studies revealed a novel mechanism that transcriptionally regulates the expression of bcl-2 in normal human endometrium.
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