| Project/Area Number |
26830079
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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 |
Tumor biology
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| Research Institution | Kumamoto University |
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Principal Investigator |
Kobayashi Daiki 熊本大学, 生命科学研究部, 非常勤教員 (20448517)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | NF1 / TCTP / プロテオミクス / 翻訳伸長因子 / EF1A2 / インタラクトミクス / 神経線維腫症1型 |
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| Outline of Final Research Achievements |
Neurofibromatosis type 1 (NF1) is an autosomal dominant disease that predisposes individuals to developing benign neurofibromas and malignant peripheral nerve sheath tumors (MPNSTs). Owing to the lack of information on the molecular mechanism of NF1-associated tumor pathogenesis, biomarkers, and therapeutic targets, a radical treatment for NF1 tumors has not been established. To analyze the function of a novel NF1-related protein, TCTP, in detail in NF1-associated tumor, we identified the TCTP-interacting proteins by proteomic approach. As a result, TCTP interacts with proteins related to protein translation mechinery and stress. Especially, TCTP specifically interacts with EF1A2, suggesting that the interaction between TCTP and EF1A2 contributes to the formation of NF1-tumor specific translational machinery. Our findings also suggest that the inhibition of TCTP-EF1A2 interaction is a therapeutic target for NF1-associated tumors.
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