2019 Fiscal Year Final Research Report
Regulation mechanism of Ras signal by novel RasGAP specific to blood cells
| Project/Area Number |
16K09822
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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 |
Hematology
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| Research Institution | Niigata University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
藤井 雅寛 新潟大学, 医歯学系, 教授 (30183099)
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| Project Period (FY) |
2016-04-01 – 2020-03-31
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| Keywords | RASAL3 / 血液腫瘍 / B細胞 / 骨髄系細胞 / 腫瘍抑制因子 |
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| Outline of Final Research Achievements |
Applicants pioneered RASAL3 as a new RasGAP in the world. In human B cell lines and myeloid tumor cell lines, forced expression of RASAL3 suppressed the development of F-actin, which is important for cell motility. B-cell and myeloid cells were abnormally proliferated in 7-9-month-old aged RASAL3-deficient mice compared with wild-type mice. Splenomegaly was frequently observed in mice lacking RASAL3. Pathological analysis of lymphoid tissue of RASAL3-deficient mice revealed pathological images suggesting abnormal proliferation and infiltration of myeloid tumor cells in bone marrow, spleen and liver. These results suggest that RASAL3 suppresses human hematological tumor cell proliferation and cell motility.
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| Free Research Field |
免疫学
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| Academic Significance and Societal Importance of the Research Achievements |
主にB細胞および骨髄系の免疫細胞においてRASAL3が血球細胞特異的な腫瘍抑制因子であることを明らかにした。この発見により、RASAL3の発現定量により将来の血液腫瘍の発症リスクを予測できるかもしれない。血液腫瘍においてRASAL3発現を回復させる薬剤が開発されれば、血液腫瘍の治療につながる可能性がある。RASAL3の機能の解明が更に進めば、B細胞および骨髄系細胞の発生、分化および増殖機構が更に明らかになる可能性がある。
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