| Project/Area Number |
26460400
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Pathological medical chemistry
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| Research Institution | Teikyo University |
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Principal Investigator |
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | ユビキチン化 / エストロゲン受容体 / ユビキチン / 乳がん |
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| Outline of Final Research Achievements |
Approximately two thirds of breast cancers grow in an estrogen-dependent fashion. Hormonal therapy, which inhibits estrogen action, has been proven effective in treatment of those breast cancers. However, resistance to such therapies often arises, complicating treatment of breast cancer patients. Estrogen signal for proliferation is transmitted into cell via estrogen receptor. Thus, it is of importance to understand fully molecular mechanism of how estrogen receptor is produced, degraded, or transferred within the cell. I have found a novel mechanism of how estrogen receptor protein is degraded: histone acetyltransferase Hbo1, involved in DNA replication, ubiquitinates estrogen receptor directly and stimulates ubiquitin-dependent proteasomal degradation. This degradation of estrogen receptor appears to contribute to cycled DNA binding and proteolysis of estrogen receptor, leading to continued activation of estrogen-dependent transcription.
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