| Project/Area Number |
16K19049
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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 |
Pathological medical chemistry
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| Research Institution | Nagoya University |
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Principal Investigator |
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | オートファジー / コンドロイチン硫酸 / PTPRσ / 軸索再生 / リン酸化・脱リン酸化 / チロシンフォスファターゼ / シグナル伝達 / 再生医学 / 神経科学 |
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| Outline of Final Research Achievements |
Upon injury, the distal terminal of axon transforms into so-called dystrophic endball. This degenerative structure has been thought to be closely associated with inability of regeneration of our axons in the cetral nervous system. However, underlying molecular mechanism except neuronal cell-surface molecule, PTPRσ, has been unknown. Here I have identified Cortactin as a new substrate for PTPRσ. Cortactin was de-phosphorylated by PTPRσ, and its phosphorylated form was completely diminished in dystrophic endball. Furthermore, knock-down of Cortactin in cultured neurons led to inhibition of axonal elongation, and swollen structures with autophagosomal accumulation which was specific character of dystrophic endball.
Taken together, these results have revealed a pivotal role of PTPRσ-Cortactin axis in axonal regeneration and its inhibition.
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