2015 Fiscal Year Final Research Report
Physiology and pathology of endocytosis and recycling transport in neurons
| Project/Area Number |
25290024
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Neurochemistry/Neuropharmacology
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| Research Institution | Tokyo Metropolitan University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
SAITO TARO 首都大学東京, 大学院理工学研究科, 助教 (70301413)
ASADA AKIKO 首都大学東京, 大学院理工学研究科, 助教 (00336512)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Keywords | タンパク質 / 酵素 / 神経科学 / 発生・分化 / Cdk5 / LMTK1 / Rab / GRAB |
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| Outline of Final Research Achievements |
Cdk5 is a brain specific membrane-bound protein kinase. We have analyzed a role of Cdk5 in neurite outgrowth in mouse primary neurons. Cdk5 phosphorylates LMTK1, a novel Ser/Thr kinase in brains, and GRAB, an activator of Rab8. Phosphorylated LMTK1 suppressed activation of Rab11 and phosphorylated GRAB lost the Rab9 activation activity. Rab11 and Rab8 are major regulators in endosome transport, supplying membrane components to the tip of axon or dendrites. Thus, their inactivation results in the reduced neurite outgrowth. This signaling cascade is negative regulatory mechanism of neurite outgrowth.
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| Free Research Field |
神経生化学
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