2006 Fiscal Year Final Research Report Summary
Molecular mechanism underlying promotion of neuronal regeneration
| Project/Area Number |
17300113
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Nerve anatomy/Neuropathology
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| Research Institution | Osaka City University |
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Principal Investigator |
KIYAMA Hiroshi Osaka City University, Graduate School of Medicine, Professor, 大学院医学研究科, 教授 (00192021)
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| Co-Investigator(Kenkyū-buntansha) |
KIRYU-SEO Sumiko (桐生 寿美子) Osaka City University, Graduate School of Medicine, Lecturer, 大学院医学研究科, 講師 (70311529)
MAEDA Mitsuyo Osaka City University, Graduate School of Medicine, Lecturer, 大学院医学研究科(平成18年8月まで), 講師 (40122080)
NAKAGOMI Saya Osaka City University, Graduate School of Medicine, Research Associate, 大学院医学研究科, 助手 (60423894)
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| Project Period (FY) |
2005 – 2006
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| Keywords | ATF3 / cJun / STAT3 / Neuronal regeneration / hypoglossal nerve / Akt |
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| Research Abstract |
This study was carried out to investigate "Molecular mechanism underlying promotion of neuronal regeneration". Two major topics were investigated : (1) Identification of transcription factors and epigenetic factors, which are associated with neuronal regeneration, (2) Identification of protein modification, which promotes neuronal regeneration. We have revealed that transcription factors such as ATF3, cJun and STAT3 were crucial to promote nerve regeneration, and further tried to understand the interaction of those transcription factors using the promoter for one of nerve regeneration associated molecules, damage induced neuronal endopeptidase DINE. This analysis demonstrated that those transcription factors seemed not to bind the promoter region directly, and instead suggested the existence of a sort of platform molecule for the assembly of those transcription factors. The transcriptional control identified in this study may be specific to nerve regeneration and would provide a novel
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transcription mechanism for the promotion of nerve regeneration. We have also attempted to identify protein modifications such as phosphorylation, methylation, and acetylation for the promotion of nerve regeneration. To identify the modified molecules in response to nerve injury, we used 2-DG electrophoresis and blotted with antibodies, which recognized a certain kinase specific phosphorylation site for instance. The candidate spots, which showed up-regulation of the modification were further analyzed by TOFMAS. We have identified pheripherin as a phosphorylated molecule by Akt in response to nerve injury. Although the functional significance of the phosphorylation is not clear, the method established in this experiment could be a good tool for the identification of the proteins, which are modified by phosphorylation, methylation, or acetylation. The results obtained in the present project provide us with a novel transcription mechanism underlying the nerve regeneration, and also provide useful tool for the identification of molecular modification by phosphorylation, methylation, and acetylation. Less
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Research Products
(30 results)
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[Journal Article] Related Articles, Links Identification and functional characterization of mouse TPO1 as a myelin membrane protein.2006
Author(s)
Fukazawa N, Ayukawa K, Nishikawa K, Ohashi H, Ichihara N, Hikawa Y, Abe T, Kudo Y, Kiyama H, Wada K, Aoki S.
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Journal Title
Brain Res. 1070
Pages: 1-14
Description
「研究成果報告書概要(和文)」より
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[Journal Article] Cell Type-Specific Intervention of Transforming Growth Factor beta/Smad Signaling Suppresses Collagen Gene Expression and Hepatic Fibrosis in Mice.2005
Author(s)
Inagaki Y, Kushida M, Higashi K, Itoh J, Higashiyama R, Hong YY, Kawada N, Namikawa K, Kiyama H, Bou-Gharios G, Watanabe T, Okazaki I, Ikeda K
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Journal Title
Gastroenterology 129
Pages: 259-268
Description
「研究成果報告書概要(和文)」より
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