Molecular and cellular mechanisms of DCX family proteins in brain development
| Project/Area Number |
23680035
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| Research Category |
Grant-in-Aid for Young Scientists (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
Neuroscience in general
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| Research Institution | Osaka Bioscience Institute |
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Principal Investigator |
KOIZUMI Hiroyuki 公益財団法人大阪バイオサイエンス研究所, 神経細胞生物学部門, 研究員 (10334335)
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| Project Period (FY) |
2011-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥28,470,000 (Direct Cost: ¥21,900,000、Indirect Cost: ¥6,570,000)
Fiscal Year 2013: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
Fiscal Year 2012: ¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2011: ¥21,970,000 (Direct Cost: ¥16,900,000、Indirect Cost: ¥5,070,000)
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| Keywords | 軸索伸長 / 神経細胞移動 / 大脳皮質発生 / 神経回路形成 / 脳梁 / 軸索輸送 / リン酸化 / 微小管結合蛋白質 / 神経科学 / 脳神経疾患 / 神経突起伸長 / 微小管 / キナーゼ |
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| Research Abstract |
Doublecortin (Dcx) and Doublecortin-like kinases (Dclk1, Dclk2) function cooperatively in cortical layer formation and axon and dendrite formation that is required for the proper neural circuit formation. DCX family proteins deficiency is associated with epilepsy.
In this project, we identified a novel target of DCLK1, MAP7D1. Depletion of MAP7D1 in cortical layer 2/3 pyramidal cells resulted in impaired axon elongation in the corpus callosum. Overexpression of unphosphorylated mutant MAP7D1, but not wild-type MAP7D1, also impaired callosal axon elongation. These results suggested that phosphorylation of MAP7D1 by DCLK1 regulate axon elongation in neurons.
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Report
(4 results)
Research Products
(13 results)
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[Journal Article]2013
Author(s)
Shin, E., Kashiwagi, Y., Kuriu, T., Iwasaki, H., Tanaka, T., Koizumi, H., Gleeson, J.G., & Okabe, S.
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Journal Title
Nat. Commun
Volume: 4
Pages: 1440-1440
Related Report
Peer Reviewed
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