A new molecular mechanism underlying receptor protein tyrosine phosphatase-mediated target recognition
| Project/Area Number |
17K14962
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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 |
Neurochemistry/Neuropharmacology
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| Research Institution | Osaka University |
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Principal Investigator |
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| Research Collaborator |
Iguchi Tokuichi
Taniguchi Manabu
Sato Makoto
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| Project Period (FY) |
2017-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2018: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2017: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 受容体型チロシンフォスファターゼ / 皮質脊髄路 / 軸索側枝 / 神経科学 |
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| Outline of Final Research Achievements |
We demonstrated that receptor protein tyrosine phosphatase (RPTP), which is known as a synaptic organizer, played roles in the formation of axon collaterals. We identified about 30 candidate RPTP interactors, and confirmed the actual interactions with regard to the several candidate molecules. We found that glycoproteins bound to RPTP through their sugar chains, and that most of the molecules interacting with RPTP exhibited a binding preference for certain splice variants of RPTP. We also revealed that knockdown of some identified molecules inhibited the formation of axon collaterals.
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| Academic Significance and Societal Importance of the Research Achievements |
脳機能を担っているのは神経細胞が作る精緻な神経回路である。したがって、神経細胞が的確な場所へと軸索を伸ばし、適切な相手とシナプスを形成するに至る「標的認識」を担う分子機構を解明することは、神経回路形成の仕組みや脳機能の基盤理解につながることが期待できる。
脳が傷害を受け神経回路が途切れると、重篤な機能障がいが生じるが、リハビリテーションを行えば代償機構によって一部の機能は回復する。代償機構を担うのは側枝形成による神経回路の再編成である。したがって、標的認識の分子機構を解明することは、代償機構を向上させ、神経機能を回復させる新たな治療法の開発につながると期待できる。
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Report
(3 results)
Research Products
(7 results)
