| Project/Area Number |
17H06870
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Genetics/Chromosome dynamics
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| Research Institution | Nara Institute of Science and Technology |
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Principal Investigator |
MOROZUMI Yuichi 奈良先端科学技術大学院大学, 先端科学技術研究科, 助教 (80571439)
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| Project Period (FY) |
2017-08-25 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2018: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | ブロモドメイン / ATAD2 / ヒストン修飾 / ES細胞 / クロマチン / ブロモドメインタンパク質 |
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| Outline of Final Research Achievements |
ATAD2 is ectopically expressed in many unrelated solid human tumours, and its association with poor prognosis in various cancers strongly suggest that ATAD2 overexpression favours malignant transformation and cancer progression. Although we previously showed that ATAD2 is involved in the regulation of chromatin dynamics in mouse embryonic stem (ES) cells, the function of ATAD2 remains elusive. In this study, we further investigated the role of ATAD2 in mouse ES cells and and found the possibility that ATAD2 is required for chromatin dynamics regulation during ES cell differentiation. In addition, we also revealed that ATPase domain of ATAD2 is responsible for its multimerization and multimerization of ATAD2 is important for its functions.
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| Academic Significance and Societal Importance of the Research Achievements |
様々ながんにおいて、その悪性度とATAD2発現量の間に正の相関がみられることから、ATAD2の過剰発現はがん患者の予後不良を引き起こすことが示唆されている。そのため、ATAD2の機能を明らかにすることは、その理解のみならずATAD2異常発現によるがん悪性化メカニズムの理解にも繋がることが期待できる。また、がん悪性化にATAD2が関わることから、ATAD2は抗がん剤の標的因子として近年注目を集めている。従って、本研究で得られた成果は、ATAD2を標的とした新たな抗がん剤やがんの治療および診断方法の開発に貢献するような基盤となることが期待される。
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