The mechanism remotely controlling Notch signaling through hemocytes
| Project/Area Number |
18K14697
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 44010:Cell biology-related
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| Research Institution | Osaka University |
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Principal Investigator |
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| Project Period (FY) |
2018-04-01 – 2022-03-31
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| Project Status |
Completed (Fiscal Year 2021)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2021: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2020: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2019: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2018: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | Notchシグナル / 血球細胞 / 貪食細胞 / レポーターアッセイ / 移植実験 / 貪食細胞の移植 / 小胞体 / Notchシグナル伝達 |
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| Outline of Final Research Achievements |
Notch signaling regulates various cell differentiation in multi-cellular organisms and its defects cause serious diseases such as cancer or neurodegeneration. Whereas the intracellular mechanisms controlling Notch signaling has well-established, little was understood about the controls received from outside the cell.
We discovered that Drosophila pecanex (pcx) was specifically essential for the ER morphogenesis within hemocytes. We also found that when pcx mutations occur in hemocytes, they newly acquire an ability to secrete Notch signaling inhibitors.
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| Academic Significance and Societal Importance of the Research Achievements |
大腸がんや乳がんといった一部のがん組織では、Notchシグナルの異常な亢進が認められており、Notchシグナルを抑制することでがん細胞の増殖を抑えられることが報告されている。したがって、Notchシグナルの抑制は、がんに対する新たな治療薬の開発という観点からも重要な課題である。本研究では、pecanex遺伝子の突然変異によって、血球細胞がNotchシグナル抑制因子を分泌する能力を獲得するという、新たな細胞シグナル破綻メカニズムを確立した。このNotchシグナル抑制因子はがんに対する新たな治療戦略としての可能性が期待できる。
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Report
(5 results)
Research Products
(8 results)
