Determination of the tyrosine phosphorylation signaling to regulate the oligodendrocyte differentiation.
| Project/Area Number |
24700387
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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 | National Institute for Basic Biology |
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Principal Investigator |
KUBOYAMA Kazuya 基礎生物学研究所, 統合神経生物学研究部門, NIBBリサーチフェロー (20619671)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 神経科学 / 脳・神経 / 蛋白質チロシンリン酸化酵素 / オリゴデンドロサイト / グリア細胞 / 脱髄疾患 / 蛋白質チロシン脱リン酸化酵素 / チロシンリン酸化 / プロテインチロシンホスファターゼ / Rho |
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| Research Abstract |
The purpose of this study was to determine the tyrosine phosphorylation signaling to regulate the oligodendrocyte differentiation and myelination in the central nervous system (CNS). The non-receptor protein tyrosine kinase Fyn, which is a member of the Src family of kinases, is known to induce oligodendrocyte development, and myelination. Here we revealed that Ptprz, which is a member of the receptor-like protein tyrosine phosphatase (RPTP) family, functions as the counterpart PTP for Fyn in the oligodendrocyte differentiation and myelination. In the study, Ptprz was found to regulate proper oligodendrocyte differentiation in early CNS development, and suppress remyelination at the injury site induced by the experimental autoimmune encephalomyelitis (EAE), through the dephosphorylation of p190RhoGAP that is phosphorylated by Fyn.
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Report
(3 results)
Research Products
(18 results)
