| Project/Area Number |
26350958
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Biomolecular chemistry
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| Research Institution | Kanazawa University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
北村 敬一郎 金沢大学, 保健学系, 教授 (80283117)
郡山 恵樹 鈴鹿医療科学大学, 薬学部, 准教授 (70397199)
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| Research Collaborator |
NODA Masaharu 基礎生物学研究所, 教授 (60172798)
SHINTANI Takafumi 基礎生物学研究所, 准教授 (10312208)
KATO Satoru 金沢大学, 健康増進科学センター, 研究協力員 (10019614)
HITOMI Kiyotaka 名古屋大学, 大学院創薬科学研究科, 教授 (00202276)
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| Project Period (FY) |
2014-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | Factor XIII-A / CNS regeneration / optic nerve / retina / cellular Factor XIII / zebrafish / activation peptide / repair / cellular FXIII / heat shock factor / transglutaminase / regeneration / neurite outgrowth / optioc nerve / activation mechanism / neurite sprouting |
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| Outline of Final Research Achievements |
Factor XIII-A (FXIII-A), also known as cellular transglutaminase, plays important roles in mediating cross-linking reactions in various tissues. Previous research has shown that FXIII-A was immediately upregulated in the fish retina and optic nerve after nerve injury. However, the activation mechanism of the FXIII-A remains unclear. Here, we investigated the activation mechanism of the FXIII-A using zebrafish CNS regeneration system. Thrombin mRNA was undetectable in zebrafish optic nerve and retina both before and after optic nerve injury. Sequence analysis of FXIII-A 5'-RACE products showed that most of clones derived from intact retina showed full sequence of FXIII-A, however, many clones derived from injured retina showed short sequences of FXIII-A which lacked exon 1-2 region. Therefore, unlike plasma FXIII-A, activation of FXIII-A in injured retina and optic nerve does not need the cleavage by thrombin, may occur the directly production of activated FXIII-A protein.
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