| Project/Area Number |
18K15762
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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 53010:Gastroenterology-related
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| Research Institution | Tokai University |
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Principal Investigator |
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| Project Period (FY) |
2018-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2019: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2018: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 非アルコール性脂肪性肝炎NASH / エピジェネティック制御 / Bcl6 / NASH / 非アルコール性脂肪性肝炎 / B cell lymphoma 6 |
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| Outline of Final Research Achievements |
We previously found that B cell lymphoma 6 (Bcl6) was involved in Nonalcoholic steatohepatitis (NASH) progression by the analysis of liver specific Bcl6 knockout mice. In this study, we tried to analyze the Bcl6 function through the epigenetic regulation to elucidate the NASH progression mechanism. We performed the biochemical purification to identify Bcl6 interactants using Bcl6-overexpressed 293T cells. BCoR and p53, which were already known to interact with Bcl6 and the new factors including zinc finger transcription factors were identified as Bcl6 interactants. We began to identify the hepatic Bcl6 interactants and confirm the relation between the epigenetic activity and NASH progression.
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| Academic Significance and Societal Importance of the Research Achievements |
NASHは、脂質代謝の破綻に起因するメタボシックシンドロームの肝臓での表現型と考えられる。NASH患者の増加が予想される一方で、未だ根本的な治療法はない。本研究ではBcl6の分子機能としてエピジェネティックな活性に注目して、NASH発症との関連性を検証することにより、NASHの適切な治療標的を見出すことができると考えた。また、学術的にも肝臓のBcl6の分子機能については不明な点が多く、新規の知見を得ることができると期待した。
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