| Project/Area Number |
26460983
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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 |
Gastroenterology
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| Research Institution | Gunma University |
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Principal Investigator |
SATO KEN 群馬大学, 医学部附属病院, 助教 (40396619)
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| Co-Investigator(Kenkyū-buntansha) |
山崎 勇一 群馬大学, 医学部附属病院, 助教 (00582404)
堀口 昇男 群馬大学, 医学部附属病院, 助教 (10550022)
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| Research Collaborator |
Satoh Tetsurou
Yoshino Satoshi
Gyao Bin
Tahara Hiroki
Nakajima Yoshimi
Ohyama Tatsuya
Takizawa Daichi
Tojima Hiroki
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| Project Period (FY) |
2014-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
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| Keywords | トランスレーショナルリサーチ / バイオテクノロジー / 癌 / マイクロアレイ |
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| Outline of Final Research Achievements |
PDIP1 regulates target gene expression through nuclear receptor that is a kind of intracellular proteins. In addition, there is a difference of the extent of liver fibrosis that is caused by the stimuli which accelerate liver fibrosis between PDIP1 knock out mice in which the function of PDIP1 is lost and wild type mice in which the function of PDIP1 is maintained. There is also a difference of the extent of liver tumor that is caused by the stimuli which induce liver tumor between PDIP1 knock out mice and wild type mice. The mechanisms of the differences of liver fibrosis and tumor were analyzed and clarified.
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| Academic Significance and Societal Importance of the Research Achievements |
マウスを用いた実験であり、必ずしもヒトにおける病態を反映するとは限らないが、今回の科研費の研究により、最近生体内エネルギー代謝調節系における機能が注目されている核内受容体転写共役活性化因子の一つであるPDIP1と肝臓の線維化や発癌のメカニズムとの関係について示すことができた。今後今回の研究を元に、多臓器の線維化や発癌モデルへの応用や、PDIP1を創薬ターゲットとした開発の端緒となる成果を示すことができたといえる。
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