| Project/Area Number |
15K18965
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
General physiology
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| Research Institution | Akita University |
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Principal Investigator |
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2016: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | CCR4-NOT複合体 / ユビキチン転移酵素 / CNOT4 / 発生 / 細胞増殖 / 心機能 / Cnot4 / 発生異常 / 細胞増殖能の低下 / PAR-CLIP / 分子生物学 |
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| Outline of Final Research Achievements |
To characterize the physiological roles of CNOT4, the CCR4-NOT complex related ubiquitin ligase, we performed the functional analyses of CNOT4 as follows. CNOT4 deficient mice or Cnot4 mutant mice showed the phenotypes of embryonic death, high perinatal mortality, dwarf, and impaired heart functions. Analyses of CNOT4 depleted or CNOT4 mutated cells showed impaired cell proliferation and reduction of cell area. To elucidate the molecular mechanisms regulated with CNOT4, we performed the global analyses of CNOT4 interacting proteins or mRNAs. Mass spectrometry analyses of CNOT4-interacting proteins indicated that the CNOT4 is likely to bind to RNA binding proteins (RBPs). Moreover, several mRNAs are detected as candidates for target of CNOT4-RBP complex.
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