2020 Fiscal Year Final Research Report
The role of transcriptional repressor ZBTB20 on premature aging and energy metabolism
| Project/Area Number |
18K06971
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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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| Review Section |
Basic Section 49010:Pathological biochemistry-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 – 2021-03-31
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| Keywords | 転写因子 / 複製ストレス / DNA損傷修復 / 代謝 / クロマチン再構築 |
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| Outline of Final Research Achievements |
We have focused on the role of new age-related genes. The original new premature aging model mouse which has been established by our unique gene-trap technology (WO 2005123918 A1) has developed obesity and been short-lived with abnormal zbtb20 gene expression located in16qC1.1-3 region. It has been reported that the abnormal gene expression of zbtb20 which is located in 3q13.31 region develops primrose syndrome and 3q13 deletions and microdeletions syndrome in human. In this research, it has been clarified and suggested that the abnormal gene expression of zbtb20 develops obesity with the enhanced lipid metabolism resulting in short-lived.
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| Free Research Field |
老年学
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| Academic Significance and Societal Importance of the Research Achievements |
最近、プリムローズ症候群について、原因遺伝子がzbtb20であり、３番染色体欠失症候群に確認される早老症と同様の病態を呈することが報告された。これまで他の研究グループらによって、中枢神経の発生過程におけるZBTB20転写抑制因子の役割が徐々に明らかにされてきた一方、生体成熟後のZBTB20の役割は未だ不明であった。本研究によって、ZBTB20が生体成熟後にエネルギー代謝の同化と異化を制御し、特に脂質代謝を制御していることを示唆する成果を得た。本研究成果は、生体成熟後のエネルギー代謝を制御する新たな分子機構の一端を解明し、短寿命の原因となる肥満の新たな制御法を示唆する成果となった。
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