Loss of hematopoietic mucin-type O-glycan causes thrombocytopenia in mice
| Project/Area Number |
24300152
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Laboratory animal science
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| Research Institution | University of Tsukuba |
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Principal Investigator |
KUDO Takashi 筑波大学, 医学医療系, 准教授 (20288062)
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| Co-Investigator(Kenkyū-buntansha) |
TAKAHASHI Satoru 筑波大学, 医学医療系, 教授 (50271896)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥17,680,000 (Direct Cost: ¥13,600,000、Indirect Cost: ¥4,080,000)
Fiscal Year 2014: ¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2012: ¥7,150,000 (Direct Cost: ¥5,500,000、Indirect Cost: ¥1,650,000)
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| Keywords | 動物 / 糖鎖 / 発生・分化 / 血小板 / 発生分化 |
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| Outline of Final Research Achievements |
Mucin function has been difficult to characterize because its structure and synthesis are complex. To address the biological role of mucin-type O-glycans in hematopoietic cells, we conditionally ablated C1galt, which is essential for synthesis of mucin-type O-glycans. Inducible, Mx1-cre-mediated C1galt conditional knockout (Mx1-C1) mice exhibited severe thrombocytopenia, giant platelets, and prolonged bleeding times.There were few proplatelets in cultured Mx1-C1 primary megakaryocytes. Moreover, the expression of hypoglycosylated GpIbα protein in Mx1-C1 megakaryocytes and platelets was greatly reduced despite the fact that expression of gpIbα transcript was unchanged. Our observations indicate that O-glycan is required for terminal megakaryocyte differentiation and platelet production and that the decrease in GpIbα in cells lacking O-glycan may be caused by increased proteolysis.
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Report
(4 results)
Research Products
(6 results)
