| Project/Area Number |
25891003
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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 |
Molecular biology
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| Research Institution | Tohoku University |
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Principal Investigator |
NAKAGAWA TADASHI 東北大学, 医学(系)研究科(研究院), 助教 (30707013)
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| Research Collaborator |
FUNAYAMA Ryo 東北大学, 大学院医学系研究科, 助教 (20452295)
HOSOGANE Masaki 東北大学, 大学院医学系研究科, 助手 (30734347)
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| Project Period (FY) |
2013-08-30 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 発生・分化 / 上皮間葉移行 / タンパク質分解 / シグナル伝達 / 上皮間葉移行 (EMT) / 蛋白質 / 細胞・組織 / 生体分子 |
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| Outline of Final Research Achievements |
Cell differentiation accompanies global gene expression change. Previous studies revealed that genes to be expressed are determined by transcription factors, but emerging evidences indicate that the general transcription machinery is also involved in gene expression change.
The general transcription machinery comprises several complexes, among which the promoter recognition complex TFIID plays a pivotal role in the selection of expressed genes. During the differentiation of myoblastic cell line and the epithelial-to-mesenchymal transition (EMT) of mammary epithelial cell line, several components of TFIID were found to be degraded by the ubiquitin-proteasome system. Induction of EMT caused the increase in an ubiquitin ligase which promoted the degradation of the TFIID component, leading to the reduction of translation-related gene expression. These results revealed a novel mechanism of regulation of the general transcription machinery by protein degradation during cell differentiation.
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