Signal characteristics of heatero-receptor coupling and generation of artificial ligand
Project/Area Number |
15K14473
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Research Category |
Grant-in-Aid for Challenging Exploratory Research
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Allocation Type | Multi-year Fund |
Research Field |
Functional biochemistry
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Research Institution | Kanazawa University |
Principal Investigator |
Matsumoto Kunio 金沢大学, がん進展制御研究所, 教授 (90201780)
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Co-Investigator(Renkei-kenkyūsha) |
SUGA Hiroaki 東京大学, 大学院理学系研究科, 教授 (00361668)
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Research Collaborator |
SAKAI Katsuya 金沢大学, がん進展制御研究所, 助教 (10523318)
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Project Period (FY) |
2015-04-01 – 2017-03-31
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Project Status |
Completed (Fiscal Year 2016)
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Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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Keywords | 細胞増殖因子 / チロシンキナーゼ / 受容体 / サイトカイン / 増殖因子受容体 / シグナル伝達 / 増殖因子 / ペプチド / HGF / MET / 特殊環状ペプチド |
Outline of Final Research Achievements |
Artificial ligands that induce the dimerization of growth factor receptors may be applicable to regenerative medicine, and generation of artificial ligands that have unique and novel biological activities may be possible. We here investigated signal activation by hetero-dimerization between different growth factor receptors. The split luciferase fusion protein system and observation of receptor molecules by atomic force microscopy were performed and determined to be appropriate for evaluation of growth factor receptor dimerization. Hetero-dimer formation between MET, RET, and IGF receptors was induced in cultured cells using FKBP/FRB fusion receptors, however, activation of these receptor and downstream signaling molecules were not seen. Combination of other growth factor receptors seemed to be required to further clarify possibility for generation of artificial ligands capable of inducing hetero-receptor dimerization and activation.
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Report
(3 results)
Research Products
(23 results)
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[Journal Article] Exome sequencing deciphers a germline MET mutation in familial epidermal growth factor receptor-mutant lung cancer.2017
Author(s)
Tode N, Kikuchi T, Sakakibara T, Hirano T, Inoue A, Ohkouchi S, Tamada T, Okazaki T, Koarai A, Sugiura H, Niihori T, Aoki Y, Nakayama K, Matsumoto K, Matsubara Y, Yamamoto M, Watanabe A, Nukiwa T, Ichinose M.
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Journal Title
Cancer Sci
Volume: 印刷中
Issue: 6
Pages: 1263-1270
DOI
Related Report
Peer Reviewed / Open Access / Acknowledgement Compliant
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[Journal Article] Non-small cell lung cancer cells acquire resistance to the ALK inhibitor alectinib by activating alternative receptor tyrosine kinases.2016
Author(s)
Isozaki H, Ichihara E, Takigawa N, Ohashi K, Ochi N, Yasugi M, Ninomiya T, Yamane H, Hotta K, Sakai K, Matsumoto K, Hosokawa S, Bessho A, Sendo T, Tanimoto M, Kiura K.
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Journal Title
Cancer Research
Volume: 76
Issue: 6
Pages: 1506-1516
DOI
Related Report
Peer Reviewed
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[Journal Article] A clinical protocol to inhibit the HGF/c-Met pathway for malignant mesothelioma with an intrapleural injection of adenoviruses expressing the NK4 gene.2015
Author(s)
Tada, Y., Hiroshima, K., Shimada, H., Morishita, N., Shirakawa, T., Matsumoto, K., Shingyoji, M., Sekine, I., Tatsumi, K. and Tagawa, M.
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Journal Title
SpringerPlus
Volume: 4
Issue: 1
Pages: 358-368
DOI
Related Report
Peer Reviewed / Open Access
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