| Project/Area Number |
24657137
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Cell biology
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| Research Institution | Nara Institute of Science and Technology |
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Principal Investigator |
KATO Jun-ya 奈良先端科学技術大学院大学, バイオサイエンス研究科, 教授 (00273839)
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| Co-Investigator(Kenkyū-buntansha) |
KATO Noriko 奈良先端科学技術大学院大学, バイオサイエンス研究科, 助教 (10252785)
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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 |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | COP9 signalosome / endocycle / COP9 シグナロソーム |
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| Outline of Final Research Achievements |
Based on the preliminary data that inactivation of the COP9 signalosome complex induced endocycle, we tried to establish the mouse model system, in which the CSN5 gene can be knocked out in a bone marrow-specific and inducible manner, but failed to obtain a clear result, concluding that the system did not work as we expected. In stead, we used an in vitro differentiation system, in which K562 cells can be differentiated into megakaryocytes in response to TPA, and found that the level of CSN5 was steady but some other CSN subunit exhibited a specific and marked change. We tested a relevant mutant of the subunit and working an invitro differentiation system using bone marrow cells isolated from conditionally-knocked-out mice. As soon as we obtain an additional results, we are planning to publish the results in a form of the scientific paper.
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