Mechanism of the nuclear retention of unspoiled RNAs that ensures proper expression of genomic information
Project/Area Number |
26290062
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Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Partial Multi-year Fund |
Section | 一般 |
Research Field |
Genome biology
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Research Institution | Kobe University |
Principal Investigator |
Sakamoto Hiroshi 神戸大学, 理学(系)研究科(研究院), 教授 (00187048)
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Co-Investigator(Kenkyū-buntansha) |
井上 邦夫 神戸大学, 理学(系)研究科(研究院), 教授 (40252415)
鈴木 穣 東京大学, 新領域創成科学研究科, 教授 (40323646)
中井 謙太 東京大学, 医科学研究所, 教授 (60217643)
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Research Collaborator |
FUKUMOTO Shoichi
AIZAWA Risuke
MIWA Takashi
TAKASAKI Teruaki
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Project Period (FY) |
2014-04-01 – 2017-03-31
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Project Status |
Completed (Fiscal Year 2016)
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Budget Amount *help |
¥17,420,000 (Direct Cost: ¥13,400,000、Indirect Cost: ¥4,020,000)
Fiscal Year 2016: ¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2015: ¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2014: ¥6,500,000 (Direct Cost: ¥5,000,000、Indirect Cost: ¥1,500,000)
|
Keywords | ゲノム機能発現 / 遺伝子発現調節 / RNAスプライシング / 核外輸送 / 品質管理 / 翻訳制御 / ゲノム / スプライシング / RNAの核外輸送 |
Outline of Final Research Achievements |
NXF-1 and CRM1 are well conserved among eukaryotes and act as nuclear export receptors for mRNAs and snRNAs, respectively. EJC is a complex formed just upstream of exon-exon junctions after pre-mRNA splicing and has various functions in RNA metabolism. Depletion of Y14, a core component of EJC, in the Nematode C. elegans, results in the cytoplasmic leakage of unspliced RNAs, which depends on CRM1 and NXF-2, an NXF-1-like protein. Analysis of C. elegans and cultured cells expressing epitope-tagged NXF-2 showed that NXF-2 interacts with both NXT-1, a nuclear export factor, and eIF4E, a translation initiation factor, and functions as a translation activator when tethered on mRNA.
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Report
(4 results)
Research Products
(10 results)
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[Journal Article] The Exon Junction Complex controls the efficient and faithful splicing of a subset of transcripts involved in mitotic cell-cycle progression.2016
Author(s)
Fukumura, K., Wakabayashi, S., Kataoka, N., Sakamoto, H., ;Suzuki, Y., ;Nakai, K., Mayeda, A., Inoue, K.
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Journal Title
International Journal of Molecular Sciences
Volume: 17
Issue: 8
Pages: 1153-1153
DOI
NAID
Related Report
Peer Reviewed / Open Access / Acknowledgement Compliant
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