2022/01/27 更新

写真a

ホウ シユウビン
侯 旭濱
HOU Xubin
所属
教育研究院 医歯学系 特任助教
医歯学総合研究科 特任助教
職名
特任助教
外部リンク

学位

  • 博士(生命科学) ( 2010年3月   東北大学 )

研究キーワード

  • アクチン

  • 眼優位性

  • 神経堤細胞

  • GABA

  • 視覚野

  • 可塑性

  • 臨界期

  • 電気生理学

  • 発生生物学

研究分野

  • ライフサイエンス / 神経科学一般

  • ライフサイエンス / 神経科学一般

経歴(researchmap)

  • 新潟大学 医歯学系   神経発達学分野   特任助教

    2016年4月 - 現在

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  • 新潟大学 医歯学系   神経発達学分野   日本学術振興会外国人特別研究員

    2014年4月 - 2016年3月

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  • 新潟大学 医歯学系   神経発達学研究室(テニュアトラック)   科学技術振興研究員

    2010年4月 - 2014年3月

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  • 東北大学加齢医学研究所   分子神経研究分野

    2005年4月 - 2010年3月

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経歴

  • 新潟大学   医歯学総合研究科   特任助教

    2016年4月 - 現在

  • 新潟大学   教育研究院 医歯学系   特任助教

    2016年4月 - 現在

学歴

  • 東北大学   生命科学研究科脳構築分野(仲村研究室) (文部科学省国費留学生)

    2005年4月 - 2010年3月

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  • 筑波大学   第二学群   生物学類

    2001年4月 - 2005年3月

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所属学協会

 

論文

  • Coactosin Promotes F-Actin Protrusion in Growth Cones Under Cofilin-Related Signaling Pathway

    Xubin Hou, Motohiro Nozumi, Harukazu Nakamura, Michihiro Igarashi, Sayaka Sugiyama

    Frontiers in Cell and Developmental Biology   9   2021年6月

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    担当区分:筆頭著者, 責任著者   掲載種別:研究論文(学術雑誌)   出版者・発行元:Frontiers Media SA  

    During brain development, axon outgrowth and its subsequent pathfinding are reliant on a highly motile growth cone located at the tip of the axon. Actin polymerization that is regulated by actin-depolymerizing factors homology (ADF-H) domain-containing family drives the formation of lamellipodia and filopodia at the leading edge of growth cones for axon guidance. However, the precise localization and function of ADF-H domain-containing proteins involved in axon extension and retraction remain unclear. We have previously shown that transcripts and proteins of coactosin-like protein 1 (COTL1), an ADF-H domain-containing protein, are observed in neurites and axons in chick embryos. Coactosin overexpression analysis revealed that this protein was localized to axonal growth cones and involved in axon extension in the midbrain. We further examined the specific distribution of coactosin and cofilin within the growth cone using superresolution microscopy, structured illumination microscopy, which overcomes the optical diffraction limitation and is suitable to the analysis of cellular dynamic movements. We found that coactosin was tightly associated with F-actin bundles at the growth cones and that coactosin overexpression promoted the expansion of lamellipodia and extension of growth cones. Coactosin knockdown in oculomotor neurons resulted in an increase in the levels of the inactive, phosphorylated form of cofilin and dysregulation of actin polymerization and axonal elongation, which suggests that coactosin promoted axonal growth in a cofilin-dependent manner. Indeed, the application of a dominant-negative form of LIMK1, a downstream effector of GTPases, reversed the effect of coactosin knockdown on axonal growth by enhancing cofilin activity. Combined, our results indicate that coactosin functions promote the assembly of protrusive actin filament arrays at the leading edge for growth cone motility.

    DOI: 10.3389/fcell.2021.660349

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  • Single-Cell Visualization Deep in Brain Structures by Gene Transfer 招待 査読

    Sayaka Sugiyama, Junko Sugi, Tomoya Iijima, Xubin Hou

    Frontiers in Neural Circuits   14   2020年11月

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    担当区分:最終著者   掲載種別:研究論文(学術雑誌)   出版者・発行元:Frontiers Media SA  

    DOI: 10.3389/fncir.2020.586043

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  • Reciprocal connectivity between secondary auditory cortical field and amygdala in mice. 査読 国際誌

    Hiroaki Tsukano, Xubin Hou, Masao Horie, Hiroki Kitaura, Nana Nishio, Ryuichi Hishida, Kuniyuki Takahashi, Akiyoshi Kakita, Hirohide Takebayashi, Sayaka Sugiyama, Katsuei Shibuki

    Scientific reports   9 ( 1 )   19610 - 19610   2019年12月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Recent studies have examined the feedback pathway from the amygdala to the auditory cortex in conjunction with the feedforward pathway from the auditory cortex to the amygdala. However, these connections have not been fully characterized. Here, to visualize the comprehensive connectivity between the auditory cortex and amygdala, we injected cholera toxin subunit b (CTB), a bidirectional tracer, into multiple subfields in the mouse auditory cortex after identifying the location of these subfields using flavoprotein fluorescence imaging. After injecting CTB into the secondary auditory field (A2), we found densely innervated CTB-positive axon terminals that were mainly located in the lateral amygdala (La), and slight innervations in other divisions such as the basal amygdala. Moreover, we found a large number of retrogradely-stained CTB-positive neurons in La after injecting CTB into A2. When injecting CTB into the primary auditory cortex (A1), a small number of CTB-positive neurons and axons were visualized in the amygdala. Finally, we found a near complete absence of connections between the other auditory cortical fields and the amygdala. These data suggest that reciprocal connections between A2 and La are main conduits for communication between the auditory cortex and amygdala in mice.

    DOI: 10.1038/s41598-019-56092-9

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  • Chondroitin Sulfate Is Required for Onset and Offset of Critical Period Plasticity in Visual Cortex 査読

    Xubin Hou, Nozomu Yoshioka, Hiroaki Tsukano, Akiko Sakai, Shinji Miyata, Yumi Watanabe, Yuchio Yanagawa, Kenji Sakimura, Kosei Takeuchi, Hiroshi Kitagawa, Takao K. Hensch, Katsuei Shibuki, Michihiro Igarashi, Sayaka Sugiyama

    SCIENTIFIC REPORTS   7 ( 1 )   12646   2017年10月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:NATURE PUBLISHING GROUP  

    Ocular dominance plasticity is easily observed during the critical period in early postnatal life. Chondroitin sulfate (CS) is the most abundant component in extracellular structures called perineuronal nets (PNNs), which surround parvalbumin-expressing interneurons (PV-cells). CS accumulates in PNNs at the critical period, but its function in earlier life is unclear. Here, we show that initiation of ocular dominance plasticity was impaired with reduced CS, using mice lacking a key CS-synthesizing enzyme, CSGalNAcT1. Two-photon in vivo imaging showed a weaker visual response of PV-cells with reduced CS compared to wild-type mice. Plasticity onset was restored by a homeoprotein Otx2, which binds the major CS-proteoglycan aggrecan and promotes its further expression. Continuous CS accumulation together with Otx2 contributed bidirectionally to both onset and offset of plasticity, and was substituted by diazepam, which enhances GABA function. Therefore, CS and Otx2 may act as common inducers of both onset and offset of the critical period by promoting PV-cell function throughout the lifetime.

    DOI: 10.1038/s41598-017-04007-x

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  • Genome-Wide Target Analyses of Otx2 Homeoprotein in Postnatal Cortex 査読

    Akiko Sakai, Ryuichiro Nakato, Yiwei Ling, Xubin Hou, Norikazu Hara, Tomoya Iijima, Yuchio Yanagawa, Ryozo Kuwano, Shujiro Okuda, Katsuhiko Shirahige, Sayaka Sugiyama

    FRONTIERS IN NEUROSCIENCE   11   2017年5月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:FRONTIERS MEDIA SA  

    Juvenile brain has a unique time window, or critical period, in which neuronal circuits are remodeled by experience. Mounting evidence indicates the importance of neuronal circuit rewiring in various neurodevelopmental disorders of human cognition. We previously showed that Otx2 homeoprotein, essential for brain formation, is recaptured during postnatal maturation of parvalbumin positive interneurons (PV cells) to activate the critical period in mouse visual cortex. Cortical Otx2 is the only interneuron-enriched transcription factor known to regulate the critical period, but its downstream targets remain unknown. Here, we used ChIP-seq (chromatin immunoprecipitation sequencing) to identify genome-wide binding sites of Otx2 in juvenile mouse cortex, and interneuron-specific RNA-seq to explore the Otx2-dependent transcriptome. Otx2-bound genes were associated with human diseases such as schizophrenia as well as critical periods. Of these genes, expression of neuronal factors involved in transcription, signal transduction and mitochondria' function was moderately and broadly affected in Otx2-deficient interneurons. In contrast to reported binding sites in the embryo, genes encoding potassium ion transporters such as K(v)3.1 had juvenile cortex-specific binding sites, suggesting that Otx2 is involved in regulating fast-spiking properties during PV cell maturation. Moreover, transcripts of oxidative resistance-1 (Oxr1), whose promoter has Otx2 binding sites, were markedly downregulated in Otx2 deficient interneurons. Therefore, an important role of Otx2 may be to protect the cells from the increased oxidative stress in fast-spiking PV cells. Our results suggest that coordinated expression of Otx2 targets promotes PV cell maturation and maintains its function in neuronal plasticity and disease.

    DOI: 10.3389/fnins.2017.00307

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  • Genome-Wide Target Analyses of Otx2 Homeoprotein in Postnatal Cortex. 査読 国際誌

    Akiko Sakai, Ryuichiro Nakato, Yiwei Ling, Xubin Hou, Norikazu Hara, Tomoya Iijima, Yuchio Yanagawa, Ryozo Kuwano, Shujiro Okuda, Katsuhiko Shirahige, Sayaka Sugiyama

    Frontiers in neuroscience   11   307 - 307   2017年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Juvenile brain has a unique time window, or critical period, in which neuronal circuits are remodeled by experience. Mounting evidence indicates the importance of neuronal circuit rewiring in various neurodevelopmental disorders of human cognition. We previously showed that Otx2 homeoprotein, essential for brain formation, is recaptured during postnatal maturation of parvalbumin-positive interneurons (PV cells) to activate the critical period in mouse visual cortex. Cortical Otx2 is the only interneuron-enriched transcription factor known to regulate the critical period, but its downstream targets remain unknown. Here, we used ChIP-seq (chromatin immunoprecipitation sequencing) to identify genome-wide binding sites of Otx2 in juvenile mouse cortex, and interneuron-specific RNA-seq to explore the Otx2-dependent transcriptome. Otx2-bound genes were associated with human diseases such as schizophrenia as well as critical periods. Of these genes, expression of neuronal factors involved in transcription, signal transduction and mitochondrial function was moderately and broadly affected in Otx2-deficient interneurons. In contrast to reported binding sites in the embryo, genes encoding potassium ion transporters such as KV3.1 had juvenile cortex-specific binding sites, suggesting that Otx2 is involved in regulating fast-spiking properties during PV cell maturation. Moreover, transcripts of oxidative resistance-1 (Oxr1), whose promoter has Otx2 binding sites, were markedly downregulated in Otx2-deficient interneurons. Therefore, an important role of Otx2 may be to protect the cells from the increased oxidative stress in fast-spiking PV cells. Our results suggest that coordinated expression of Otx2 targets promotes PV cell maturation and maintains its function in neuronal plasticity and disease.

    DOI: 10.3389/fnins.2017.00307

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  • Coactosin accelerates cell dynamism by promoting actin polymerization 査読

    Xubin Hou, Tatsuya Katahira, Kazumasa Ohashi, Kensaku Mizuno, Sayaka Sugiyama, Harukazu Nakamura

    DEVELOPMENTAL BIOLOGY   379 ( 1 )   53 - 63   2013年7月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:ACADEMIC PRESS INC ELSEVIER SCIENCE  

    During development, cells dynamically move or extend their processes, which are achieved by actin dynamics. In the present study, we paid attention to Coactosin, an actin binding protein, and studied its role in actin dynamics. Coactosin was associated with actin and Capping protein in neural crest cells and N1E-115 neuroblastoma cells. Accumulation of Coactosin to cellular processes and its association with actin filaments prompted us to reveal the effect of Coactosin on cell migration. Coactosin overexpression induced cellular processes in cultured neural crest cells. In contrast, knock-down of Coactosin resulted in disruption of actin polymerization and of neural crest cell migration. Importantly, Coactosin was recruited to lamellipodia and filopodia in response to Rac signaling, and mutated Coactosin that cannot bind to F-actin did not react to Rac signaling, nor support neural crest cell migration. It was also shown that deprivation of Rac signaling from neural crest cells by dominant negative Rac1 (DN-Rac1) interfered with neural crest cell migration, and that co-transfection of DN-Rac1 and Coactosin restored neural crest cell migration. From these results we have concluded that Coactosin functions downstream of Rac signaling and that it is involved in neurite extension and neural crest cell migration by actively participating in actin polymerization. (C) 2013 Elsevier Inc. All rights reserved.

    DOI: 10.1016/j.ydbio.2013.04.006

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  • Optogenetic Probing and Manipulation of the Calyx-Type Presynaptic Terminal in the Embryonic Chick Ciliary Ganglion 査読

    Ryo Egawa, Shoko Hososhima, Xubin Hou, Hidetaka Katow, Toru Ishizuka, Harukazu Nakamura, Hiromu Yawo

    PLOS ONE   8 ( 3 )   e59179   2013年3月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:PUBLIC LIBRARY SCIENCE  

    The calyx-type synapse of chick ciliary ganglion (CG) has been intensively studied for decades as a model system for the synaptic development, morphology and physiology. Despite recent advances in optogenetics probing and/or manipulation of the elementary steps of the transmitter release such as membrane depolarization and Ca2+ elevation, the current gene-manipulating methods are not suitable for targeting specifically the calyx-type presynaptic terminals. Here, we evaluated a method for manipulating the molecular and functional organization of the presynaptic terminals of this model synapse. We transfected progenitors of the Edinger-Westphal (EW) nucleus neurons with an EGFP expression vector by in ovo electroporation at embryonic day 2 (E2) and examined the CG at E8-14. We found that dozens of the calyx-type presynaptic terminals and axons were selectively labeled with EGFP fluorescence. When a Brainbow construct containing the membrane-tethered fluorescent proteins m-CFP, m-YFP and m-RFP, was introduced together with a Cre expression construct, the color coding of each presynaptic axon facilitated discrimination among inter-tangled projections, particularly during the developmental re-organization period of synaptic connections. With the simultaneous expression of one of the chimeric variants of channelrhodopsins, channelrhodopsin-fast receiver (ChRFR), and R-GECO1, a red-shifted fluorescent Ca2+-sensor, the Ca2+ elevation was optically measured under direct photostimulation of the presynaptic terminal. Although this optically evoked Ca2+ elevation was mostly dependent on the action potential, a significant component remained even in the absence of extracellular Ca2+. It is suggested that the photo-activation of ChRFR facilitated the release of Ca2+ from intracellular Ca2+ stores directly or indirectly. The above system, by facilitating the molecular study of the calyx-type presynaptic terminal, would provide an experimental platform for unveiling the molecular mechanisms underlying the morphology, physiology and development of synapses.

    DOI: 10.1371/journal.pone.0059179

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  • Conditional knockdown of target gene expression by tetracycline regulated transcription of double strand RNA 査読

    Xubin Hou, Minoru Omi, Hidekiyo Harada, Shunsuke Ishii, Yoshiko Takahashi, Harukazu Nakamura

    DEVELOPMENT GROWTH & DIFFERENTIATION   53 ( 1 )   69 - 75   2011年1月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:WILEY-BLACKWELL PUBLISHING, INC  

    In vivo electroporation has served as an effective tool for the study of developmental biology. Here we report tetracycline inducible gene knockdown by electroporation. Our system consists of genome integration of a cassette encoding long double strand RNA (dsRNA) of a gene of interest by electroporation, transcription of which is assured by RNA polymerase II, and induction of transcription of dsRNA by tetracyclin. Long dsRNA decapped by ribozyme in the cassette and without poly A tail is processed into siRNA within nuclei. We could successfully induce knockdown of En2 and Coactosin by Dox administration.

    DOI: 10.1111/j.1440-169X.2010.01229.x

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  • Expression of chick Coactosin in cells in morphogenetic movement 査読

    Xubin Hou, Tatsuya Katahira, Jun Kimura, Harukazu Nakamura

    DEVELOPMENT GROWTH & DIFFERENTIATION   51 ( 9 )   833 - 840   2009年12月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:WILEY-BLACKWELL PUBLISHING, INC  

    Coactosin is a 17 kDa actin binding protein that belongs to the actin depolymerizing factor/cofilin homology family. Coactosin inhibits barbed-end capping of actin filament, and is involved in actin polymerization. Coactosin is expressed in cephalic and trunk neural crest cells, cranial ganglia and dorsal root ganglia. Coactosin is also expressed in the cells that are forming mesonephric duct, and endodermal cells. Immunocytochemistry with anti-Coactosin antibody shows that Coactosin is localized in the cytoplasm, and associated with actin stress fibers in cultured neural crest cells. Coactosin is also expressed in the axon of oculomotor nerve and trigeminal nerve. In the growth cone of the oculomotor nerve axons, both Coactosin mRNA and protein were localized, which is indicative of the role of Coactosin in pathfinding of the growth cone. Coactosin is expressed in those that require dynamic and highly coordinated regulation of actin cytoskeleton, that is, neural crest cells, cells in the tip of the mesonephros, endodermal cells and axons.

    DOI: 10.1111/j.1440-169X.2009.01146.x

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  • In Ovo electroporation as a useful tool to pursue molecular mechanisms of neural development in chick embryos 査読

    Noritaka Odani, Xubin Hou, Harukazu Nakamura

    Electroporation and Sonoporation in Developmental Biology   9 - 16   2009年

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    記述言語:英語   掲載種別:論文集(書籍)内論文   出版者・発行元:Springer Japan  

    In the field of developmental biology, electroporation has become a routine technique for gene transfer because of its simplicity and wide range of application. In chick embryos, the in ovo electroporation technique has enabled molecular analysis of developmental mechanisms in chick embryos and has revived chick embryos as the model animals in developmental biology (Muramatsu et al., 1997
    Sakamoto et al., 1998
    Funahashi et al., 1999
    Nakamura et al., 2000). Especially, many gene analyses were conducted in developing neural tube, because the neural tube is a convenient tissue for application of in ovo electroporation. Here, we show the application of in ovo electroporation to the developmental neural tube in chick embryo. electroporation, only the anode side is transfected and the cathode side could be used as the control (Funahashi et al., 1999
    Nakamura et al., 2000
    Odani et al., 2008). © 2009 Springer Japan.

    DOI: 10.1007/978-4-431-09427-2_2

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書籍等出版物

  • Electroporation and Sonoporation in Developmental Bilogy

    Odani Noritaka, Xubin Hou, Harukazu Nakamura, Nakamura Harukazu( 担当: 分担執筆 ,  範囲: In ovo electroporation as a strong tool to pursue molecular mechanisms of neural development in chick)

    Springer  2009年4月  ( ISBN:4431094261

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    総ページ数:364  

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MISC

  • 弱視の臨界期に関する最近の知見 招待 査読

    杉山清佳, 侯旭濱

    眼科   61 ( 1 )   2019年1月

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  • 生後の抑制性介在ニューロン発達におけるホメオタンパク質Otx2の網羅的ターゲット解析

    酒井晶子, 中戸隆一郎, LING Yiwei, HOU Xubin, 原範和, 飯島友也, 柳川右千夫, 桑野良三, 奥田修二郎, 白髭克彦, 杉山清佳

    エピゲノムはどこまで操れるようになったか 第11回日本エピジェネティクス研究会年会プログラム集 理研シンポジウム 平成29年   105   2017年

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    記述言語:日本語  

    J-GLOBAL

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  • Localization of the actin binding protein, coactosin that expressed in the developing chick ciliary ganglion

    Shoko Hososhima, Xubin Hou, Toru Isizuka, Harukazu Nakamura, Hiromu Yawo

    NEUROSCIENCE RESEARCH   71   E333 - E333   2011年

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:ELSEVIER IRELAND LTD  

    DOI: 10.1016/j.neures.2011.07.1456

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  • Upregulation of an actin binding protein, Coactosin during maturation of parvalbumin-positive interneurons in mouse visual cortex

    Xubin Hou, Sayaka Sugiyama

    NEUROSCIENCE RESEARCH   71   E132 - E132   2011年

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:ELSEVIER IRELAND LTD  

    DOI: 10.1016/j.neures.2011.07.565

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  • Optical imaging of exocytosis from the calyx-type presynaptic terminal of the chick ciliary ganglion with novel red fluorescence exocyotosis probe, VAMP-mOrange

    Ryo Egawa, Saki Tanimoto, Shoko Hososhima, Xubin Hou, Seiichiro Sakai, Toru Ishizuka, Harukazu Nakamura, Hiromu Yawo

    JOURNAL OF PHYSIOLOGICAL SCIENCES   60   S126 - S126   2010年

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:SPRINGER TOKYO  

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  • Genetic manipulation of molecular organization and function of the calyx-type presynaptic terminal in the chick ciliary ganglion

    Ryo Egawa, Saki Tanimoto, Shoko Hososhima, Xubin Hou, Seiichirou Sakai, Toru Ishizuka, Harukazu Nakamura, Hiromu Yawo

    NEUROSCIENCE RESEARCH   68   E234 - E234   2010年

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:ELSEVIER IRELAND LTD  

    DOI: 10.1016/j.neures.2010.07.1035

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講演・口頭発表等

  • Coordinated regulation of neural network by inhibitory and excitatory neurons

    Sayaka Sugiyama, Xubin Hou

    The 39th Annual Meeting of the Japan Neuroscience Society  2016年 

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  • 臨界期の時期を制御する分子たち

    杉山清佳, 侯, 旭濱

    視覚科学フォーラム 第18回 特別企画シンポジウム  2014年 

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  • Conditional knockdown of target gen expression: Tet-on of transcription of double strand RNA

    Xubin Hou

    Chick 7: Avian Model System (7th International Chick Meeting)  2012年 

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  • アクチン結合蛋白Coactosin: 神経堤細胞移動における解析

    侯 旭濱, 仲村春和

    第14回東北大脳科学グローバルCOE若手フォーラム  2009年 

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  • Analysis of Coactosin, an actin binding protein, in neural crest cell migration

    侯 旭濱

    Japan-China Joint Neuroscience Workshop for Young Scientists  2008年 

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  • Analysis of Coactosin, an actin binding protein, in neural crest cell migration

    Xubin Hou, Harukazu Nakamura

    5th International Chick Meeting  2007年 

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受賞

  • 生命科学研究科長賞

    2010年2月   東北大学  

    侯 旭濱

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  • 藤野先生記念奨励賞(魯迅賞)

    2006年12月   東北大学  

    侯 旭濱

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共同研究・競争的資金等の研究

  • 経験による皮質抑制性ニューロン局所回路形成と情報処理機構の解明

    研究課題/領域番号:20K06869  2020年4月 - 2023年3月

    日本学術振興会  科学研究費助成事業 基盤研究(C)  基盤研究(C)

    侯 旭濱, 菱田 竜一

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    配分額:4290000円 ( 直接経費:3300000円 、 間接経費:990000円 )

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  • アクチン再構築による臨界期制御機構の解析

    2016年 - 2018年

    研究活動スタート支援 

    侯 旭濱

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    担当区分:研究代表者  資金種別:競争的資金

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  • アクチン再構築による臨界期制御メカニズム解析

    2014年 - 2016年

    特別研究員奨励費 (JSPS外国人特別研究員) 

    侯 旭濱

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    担当区分:研究代表者  資金種別:競争的資金

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  • アクチン再構築による臨界期制御メカニズムの解析

    2014年

    若手研究(B) 

    侯 旭濱

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    担当区分:研究代表者  資金種別:競争的資金

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  • 臨界期におけるホメオ蛋白質の翻訳制御機構の解析

    2013年 - 2014年

    新潟大学  新潟大学プロジェクト推進奨励研究 

    侯 旭濱

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    担当区分:研究代表者  資金種別:競争的資金

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  • シナプス前終末における小胞プールダイナミクス可塑性の研究

    2009年 - 2010年

    東北大学GCOE異分野融合特別研究奨励費 

    侯 旭濱

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    担当区分:研究代表者  資金種別:競争的資金

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▶ 全件表示