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70 results on '"神野, 尚三"'

1. 高次脳機能の制御基盤としての海馬の糖鎖.

Author

神野 尚三

Abstract

Copyright of Seikagaku Journal of Japanese Biochemical is the property of Japanese Biochemical Society and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Published
2024
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38. miR-214 は統合失調症関連遺伝子 Quaking （Qki）を標的としてニューロンにおける樹状突起の形成を促進する

Author

Hideyuki Nakashima, Keita Tsujimura, Kinichi Nakashima, Koichiro Irie, 神野, 尚三, 神庭, 重信, and 吉良, 潤一

Subjects
0301 basic medicine, Untranslated region, neurite outgrowth, Synaptogenesis, Morphogenesis, Down-Regulation, Biology, Biochemistry, dendrite, 03 medical and health sciences, microRNA (miRNA), Mice, Neurobiology, microRNA, Animals, Molecular Biology, Gene, Genetics, Messenger RNA, Gene knockdown, neurodevelopment, RNA-Binding Proteins, Cell Biology, Dendrites, RNA binding protein, Axons, Cell biology, Dendrite morphogenesis, MicroRNAs, 030104 developmental biology, Synapses, Schizophrenia
Abstract

Proper dendritic elaboration of neurons is critical for the formation of functional circuits during brain development. Defects in dendrite morphogenesis are associated with neuropsychiatric disorders, and microRNAs are emerging as regulators of aspects of neuronal maturation such as axonal and dendritic growth, spine formation, and synaptogenesis. Here, we show that miR-214 plays a pivotal role in the regulation of dendritic development. Overexpression of miR-214 increased dendrite size and complexity, whereas blocking of endogenous miR-214-3p, a mature form of miR-214, inhibited dendritic morphogenesis. We also found that miR-214-3p targets quaking (Qki), which is implicated in psychiatric diseases such as schizophrenia, through conserved target sites located in the 3'-untranslated region of Qki mRNA, thereby down-regulating Qki protein levels. Overexpression and knockdown of Qki impaired and enhanced dendritic formation, respectively. Moreover, overexpression of Qki abolished the dendritic growth induced by miR-214 overexpression. Taken together, our findings reveal a crucial role for the miR-214-Qki pathway in the regulation of neuronal dendritic development.

Published
2017

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