| Project/Area Number |
18592029
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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 |
Functional basic dentistry
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| Research Institution | Osaka University |
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Principal Investigator |
SAEKI Makio Osaka University, Graduate School of Dentistry, Pharmacology, Assistant Professor (30273692)
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| Co-Investigator(Kenkyū-buntansha) |
KAMISAKI Yoshinori Osaka University, Graduate School of Dentistry Pharmacology, Professor (40116017)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥3,800,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥300,000)
Fiscal Year 2007: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2006: ¥2,500,000 (Direct Cost: ¥2,500,000)
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| Keywords | apoptosis / calcineurin / caspase / cell death / 遺伝子 / 酵素 / 細胞・組織 / 歯学 / シグナル伝達 |
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| Research Abstract |
Overexpression of calcineurin B in HEK 293 cells potentiated processing of caspase-3 and apoptosis triggered by tumor necrosis factor-α and cycloheximide treatment. In a cell-free system, overexpression of calcineurin B in HEK 293 cells markedly increased processing of caspase-3 by cytochrome c. Immunodepletion of calcineurin B from cytosolic extracts from Jurkat cells decreased processing of caspase-3 by cytochrome c. Knockdown of calcineurin B by RNA interference resulted in a reduced apoptosis in HEK293 cells, but not in caspase-3-deficient MCF-7 cells. These results suggest that calcineurin B may possess a novel function to participate in the regulation of apoptosis, in addition to its well-known ability to regulate calcineurin A. Furthermore, calcineurin B itself has no effect on apoptosis, but promotes apoptotic signal transduction system through the presentation of scaffold for the activation of caspase-3 by caspase-9. Therefore, calcineurin B may be useful for therapies to induce and promote apoptosis.
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