Details of the Researcher

PHOTO

Nariko Arimura
Section
Graduate School of Pharmaceutical Sciences
Job title
Associate Professor
Degree

  • 博士（医学）（名古屋大学）

  • 修士（バイオサイエンス）（奈良先端科学技術大学院大学）

Profile

個人のホームページ　　https://arimura97.wixsite.com/my-site2025/home

Research History 8

  • 2022/04 - Present
    Tohoku University　Department of Pharmacology, Graduate School of Pharmaceutical Sciences　Associate Professor

  • 2020/04 - Present
    National Center of Neurology and Psychiatry　Research Fellow

  • 2017/04 - 2020/03
    JSPS Research Fellow (RPD)

  • 2013 - 2017
    Research Fellow, National Institute of Neuroscience, National Center of Neurology and Psychiatry

  • 2011 - 2012
    Senior Researcher, Tokyo Metropolitan Institute of Medical Science

  • 2008 - 2011
    GCOE Associate Professor, Brain Science Institute, Tamagawa University

  • 2005 - 2008
    Assistant Professor, Medical Education Research Support Center, Graduate School of MedicineNagoya University

  • 2003 - 2004
    JSPS Research Fellow (PD)

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Education 4

  • Nagoya University Graduate School of Medicine　PhD

    2000 - 2003

  • Nara Institute of Science and Technology Division of Biological Science　M.Sc

    1998 - 2000

  • Department of Biology, Faculty of Science, Kyusyu University　B.Sc

    1994 - 1998

  • Reimei Senior High School

    - 1994

Committee Memberships 6

  • Discover Neuroscience (Springer Nature)　Editorial Board Members, Section Editor

    2025/01 - Present

  • Frontiers in Neuroscience　the board of Neuroscience Methods and Techniques, Associate Editor

    2024/02 - Present

  • The Japanese Society for Neurochemistry　Councilor

    2022/04 - Present

  • 日本神経化学会　ダイバーシティー推進委員会 委員

    2021/06 - Present

  • Frontiers in Genetics, Neuroscience, and Neurology　the board of Neurogenomics, Associate Editor

    2022/10 - 2024/09

  • 日本神経化学会　シンポジウム企画委員会 委員

    2021/06 - 2023/05

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Professional Memberships 8

  • The Pharmaceutical Society of Japan

    2023/01 - Present

  • The Japanese Pharmacological Society

    2023/01 - Present

  • The Japanese Society of Neuropsypharmacology

    2022/03 - Present

  • The Japanese Biochemical Society

    2020/02 - 2023/07

  • Molecular Biology Society of Japan

    2016/07 -

  • The Japan Neuroscience Society

    2006/04 -

  • The Japanese Society for Neurochemistry

  • Society for Neuroscience

︎Show all ︎Show first 5

Research Interests 12

  • Glial cell

  • brain injury

  • dementia

  • CRMP-2

  • Dscam

  • Basal ganglia

  • The midbrain development

  • Neuronal development

  • Cerebral physiology

  • Biochemistry

  • Molecular Biology

  • Neuroscience

Research Areas 7

  • Life sciences / Pathobiochemistry /

  • Life sciences / Psychiatry /

  • Life sciences / Functional biochemistry /

  • Life sciences / Neuroscience - general /

  • Life sciences / Cell biology /

  • Life sciences / Developmental biology /

  • Humanities & social sciences / Cognitive sciences /

Papers 41

  1. A method to analyze gene expression profiles from hippocampal neurons electrophysiologically recorded in vivo

    Haruya Yagishita, Yasuhiro Go, Kazuki Okamoto, Nariko Arimura, Yuji Ikegaya, Takuya Sasaki

    Frontiers in Neuroscience　18　2024/04/17

    Publisher: Frontiers Media SA

    DOI： 10.3389/fnins.2024.1360432 　

    eISSN： 1662-453X

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    Hippocampal pyramidal neurons exhibit diverse spike patterns and gene expression profiles. However, their relationships with single neurons are not fully understood. In this study, we designed an electrophysiology-based experimental procedure to identify gene expression profiles using RNA sequencing of single hippocampal pyramidal neurons whose spike patterns were recorded in living mice. This technique involves a sequence of experiments consisting of in vivo juxtacellular recording and labeling, brain slicing, cell collection, and transcriptome analysis. We demonstrated that the expression levels of a subset of genes in individual hippocampal pyramidal neurons were significantly correlated with their spike burstiness, submillisecond-level spike rise times or spike rates, directly measured by in vivo electrophysiological recordings. Because this methodological approach can be applied across a wide range of brain regions, it is expected to contribute to studies on various neuronal heterogeneities to understand how physiological spike patterns are associated with gene expression profiles.

  2. Neuronal DSCAM regulates the peri-synaptic localization of GLAST in Bergmann glia for functional synapse formation

    Ken-ichi Dewa, Nariko Arimura, Wataru Kakegawa, Masayuki Itoh, Toma Adachi, Satoshi Miyashita, Yukiko U. Inoue, Kento Hizawa, Kei Hori, Natsumi Honjoya, Haruya Yagishita, Shinichiro Taya, Taisuke Miyazaki, Chika Usui, Shoji Tatsumoto, Akiko Tsuzuki, Hirotomo Uetake, Kazuhisa Sakai, Kazuhiro Yamakawa, Takuya Sasaki, Jun Nagai, Yoshiya Kawaguchi, Masaki Sone, Takayoshi Inoue, Yasuhiro Go, Noritaka Ichinohe, Kozo Kaibuchi, Masahiko Watanabe, Schuichi Koizumi, Michisuke Yuzaki, Mikio Hoshino

    Nature Communications　15　(1)　2024/02/01

    Publisher: Springer Science and Business Media LLC

    DOI： 10.1038/s41467-023-44579-z 　

    eISSN： 2041-1723

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    Abstract In the central nervous system, astrocytes enable appropriate synapse function through glutamate clearance from the synaptic cleft; however, it remains unclear how astrocytic glutamate transporters function at peri-synaptic contact. Here, we report that Down syndrome cell adhesion molecule (DSCAM) in Purkinje cells controls synapse formation and function in the developing cerebellum. Dscam-mutant mice show defects in CF synapse translocation as is observed in loss of function mutations in the astrocytic glutamate transporter GLAST expressed in Bergmann glia. These mice show impaired glutamate clearance and the delocalization of GLAST away from the cleft of parallel fibre (PF) synapse. GLAST complexes with the extracellular domain of DSCAM. Riluzole, as an activator of GLAST-mediated uptake, rescues the proximal impairment in CF synapse formation in Purkinje cell-selective Dscam-deficient mice. DSCAM is required for motor learning, but not gross motor coordination. In conclusion, the intercellular association of synaptic and astrocyte proteins is important for synapse formation and function in neural transmission.

  3. A Comparative Overview of DSCAM and its Multifunctional Roles in Drosophila and Vertebrates

    Kento Hizawa, Takuya Sasaki, Nariko Arimura

    Neuroscience Research　2024/02

    Publisher: Elsevier BV

    DOI： 10.1016/j.neures.2023.12.005 　

    ISSN： 0168-0102

  4. Novel FABP3 ligand, HY-11-9, ameliorates neuropathological deficits in MPTP-induced Parkinsonism in mice Peer-reviewed

    Haoyang Wang, Kohji Fukunaga, An Cheng, Yifei Wang, Nariko Arimura, Hiroshi Yoshino, Takuya Sasaki, Ichiro Kawahata

    Journal of Pharmacological Sciences　152　(1)　30-38　2023/03

    DOI： 10.1016/j.jphs.2023.02.008 　

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    Parkinson's disease (PD) is characterized by dopaminergic (DAergic) neuronal loss in the substantia nigra pars compacta (SNpc), resulting from α-synuclein (αSyn) toxicity. We previously reported that αSyn oligomerization and toxicity are regulated by the fatty-acid binding protein 3 (FABP3), and the therapeutic effects of the FABP3 ligand, MF1, was successfully demonstrated in PD models. Here, we developed a novel and potent ligand, HY-11-9, which has a higher affinity for FABP3 (Kd = 11.7 ± 8.8) than MF1 (Kd = 302.8 ± 130.3). We also investigated whether the FABP3 ligand can ameliorate neuropathological deterioration after the onset of disease in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced Parkinsonism. Motor deficits were observed two weeks after MPTP treatment. Notably, oral administration of HY-11-9 (0.03 mg/kg) improved motor deficits in both beam-walking and rotarod tasks, whereas MF1 failed to improve the motor deficits in both tasks. Consistent with the behavioral tasks, HY-11-9 recovered dopamine neurons from MPTP toxicity in the substantia nigra and ventral tegmental areas. Furthermore, HY-11-9 reduced the accumulation of phosphorylated-serine129-α-synuclein (pS129-αSyn) and colocalization with FABP3 in tyrosine hydroxylase (TH)-positive DA neurons in the PD mouse model. Overall, HY-11-9 significantly improved MPTP-induced behavioral and neuropathological deterioration, suggesting that it may be a potential candidate for PD therapy.

  5. Neuronal and Astrocytic Protein Connections and Associated Adhesion Molecules Peer-reviewed

    Kenichi Dewa, Nariko Arimura

    Neuroscience Research　187　14-20　2023/02

    DOI： 10.1016/j.neures.2022.09.014 　

  6. AUTS2 Governs Cerebellar Development, Purkinje Cell Maturation, Motor Function and Social Communication. International-journal

    Kunihiko Yamashiro, Kei Hori, Esther S K Lai, Ryo Aoki, Kazumi Shimaoka, Nariko Arimura, Saki F Egusa, Asami Sakamoto, Manabu Abe, Kenji Sakimura, Takaki Watanabe, Naofumi Uesaka, Masanobu Kano, Mikio Hoshino

    iScience　23　(12)　101820-101820　2020/12/18

    DOI： 10.1016/j.isci.2020.101820 　

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    Autism susceptibility candidate 2 (AUTS2), a risk gene for autism spectrum disorders (ASDs), is implicated in telencephalon development. Because AUTS2 is also expressed in the cerebellum where defects have been linked to ASDs, we investigated AUTS2 functions in the cerebellum. AUTS2 is specifically localized in Purkinje cells (PCs) and Golgi cells during postnatal development. Auts2 conditional knockout (cKO) mice exhibited smaller and deformed cerebella containing immature-shaped PCs with reduced expression of Cacna1a. Auts2 cKO and knock-down experiments implicated AUTS2 participation in elimination and translocation of climbing fiber synapses and restriction of parallel fiber synapse numbers. Auts2 cKO mice exhibited behavioral impairments in motor learning and vocal communications. Because Cacna1a is known to regulate synapse development in PCs, it suggests that AUTS2 is required for PC maturation to elicit normal development of PC synapses and thus the impairment of AUTS2 may cause cerebellar dysfunction related to psychiatric illnesses such as ASDs.

  7. DSCAM regulates delamination of neurons in the developing midbrain Peer-reviewed

    Nariko Arimura, Mako Okada, Shinichiro Taya, Ken-ichi Dewa, Akiko Tsuzuki, Hirotomo Uetake, Satoshi Miyashita, Koichi Hashizume, Kazumi Shimaoka, Saki Egusa, Tomoki Nishioka, Yuchio Yanagawa, Kazuhiro Yamakawa, Yukiko U. Inoue, Takayoshi Inoue, Kozo Kaibuchi, Mikio Hoshino

    Science Advances　6　(36)　eaba1693-eaba1693　2020/09

    Publisher: American Association for the Advancement of Science (AAAS)

    DOI： 10.1126/sciadv.aba1693 　

    eISSN： 2375-2548

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    For normal neurogenesis and circuit formation, delamination of differentiating neurons from the proliferative zone must be precisely controlled; however, the regulatory mechanisms underlying cell attachment are poorly understood. Here, we show that Down syndrome cell adhesion molecule (DSCAM) controls neuronal delamination by local suppression of the RapGEF2–Rap1–N-cadherin cascade at the apical endfeet in the dorsal midbrain. <italic>Dscam</italic> transcripts were expressed in differentiating neurons, and DSCAM protein accumulated at the distal part of the apical endfeet. Cre-<italic>loxP</italic>–based neuronal labeling revealed that <italic>Dscam</italic> knockdown impaired endfeet detachment from ventricles. DSCAM associated with RapGEF2 to inactivate Rap1, whose activity is required for membrane localization of N-cadherin. Correspondingly, <italic>Dscam</italic> knockdown increased N-cadherin localization and ventricular attachment area at the endfeet. Furthermore, excessive endfeet attachment by <italic>Dscam</italic> knockdown was restored by co-knockdown of <italic>RapGEF2</italic> or <italic>N-cadherin</italic>. Our findings shed light on the molecular mechanism that regulates a critical step in early neuronal development.

  8. Comprehensive and cell-type-based characterization of the dorsal midbrain during development. International-journal Peer-reviewed

    Arimura N, Dewa KI, Okada M, Yanagawa Y, Taya SI, Hoshino M

    Genes to cells : devoted to molecular & cellular mechanisms　24　(1)　41-59　2019/01

    DOI： 10.1111/gtc.12656 　

    ISSN： 1356-9597

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    The layer structure has been intensively characterized in the developing neocortex and cerebellum based on the various molecular markers. However, as to the developing dorsal midbrain, comprehensive analyses have not been intensely carried out, and thus, the name as well as the definition of each layer is not commonly shared. Here, we redefined the three layers, such as the ventricular zone, intermediate zone and marginal zone, based on various markers for proliferation and differentiation in embryonic dorsal midbrain. Biphasic Ki67 expression defines the classical VZ, in which there is clear separation of the mitotic and interphase zones. Next, we mapped the distribution of immature neurons to the defined layers, based on markers for glutamatergic and GABAergic lineage. Interestingly, Tbr2 and Neurog2 were expressed in the postmitotic neurons. We also report that active (phosphorylated) JNK is a useful marker to demarcate layers during the embryonic stage. Finally, we validated the final arrival layers of the migratory glutamatergic and GABAergic neurons. These results form a foundation for analyses of brain development, especially in the proliferation and migration of excitatory and inhibitory neurons in the dorsal midbrain.

  9. TTBK2 with EB1/3 regulates microtubule dynamics in migrating cells through KIF2A phosphorylation Peer-reviewed

    Takashi Watanabe, Mai Kakeno, Toshinori Matsui, Ikuko Sugiyama, Nariko Arimura, Kenji Matsuzawa, Aya Shirahige, Fumiyoshi Ishidate, Tomoki Nishioka, Shinichiro Taya, Mikio Hoshino, Kozo Kaibuchi

    JOURNAL OF CELL BIOLOGY　210　(5)　737-751　2015/08

    DOI： 10.1083/jcb.201412075 　

    ISSN： 0021-9525

    eISSN： 1540-8140

  10. Involvement of the Globus Pallidus in Behavioral Goal Determination and Action Specification Peer-reviewed

    Nariko Arimura, Yoshihisa Nakayama, Tomoko Yamagata, Jun Tanji, Eiji Hoshi

    JOURNAL OF NEUROSCIENCE　33　(34)　13639-13653　2013/08

    DOI： 10.1523/JNEUROSCI.1620-13.2013 　

    ISSN： 0270-6474

  11. Local Application of Neurotrophins Specifies Axons Through Inositol 1,4,5-Trisphosphate, Calcium, and Ca2+/Calmodulin-Dependent Protein Kinases Peer-reviewed

    Shinichi Nakamuta, Yasuhiro Funahashi, Takashi Namba, Nariko Arimura, Marina R. Picciotto, Hiroshi Tokumitsu, Thomas R. Soderling, Akira Sakakibara, Takaki Miyata, Hiroyuki Kamiguchi, Kozo Kaibuchi

    SCIENCE SIGNALING　4　(199)　2011/11

    DOI： 10.1126/scisignal.2002011 　

    ISSN： 1937-9145

  12. [Neural mechanisms underlying the integration of perception and action]. Peer-reviewed

    Eiji Hoshi, Yoshihisa Nakayama, Tomoko Yamagata, Yosuke Saga, Masashi Hashimoto, Nariko Arimura, Jun Tanji

    Brain and nerve = Shinkei kenkyu no shinpo　63　(1)　59-68　2011/01

    ISSN： 1881-6096

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    The hallmark of higher-order brain functions is the ability to integrate and associate diverse sets of information in a flexible manner. Thus, fundamental knowledge about the mechanisms underlying of information in the brain can be obtained by examining the neural mechanisms involved in the generation of an appropriate motor command based on perceived sensory signals. In this review article, we have focused on the involvement of the neuronal networks centered at the lateral aspect of the frontal cortex in the process of motor selection and motor planning based on visual signals. We have initially discussed the role of the lateral prefrontal cortex in integrating multiple sets of visual signals to select a reach target and the participation of the premotor cortex in retrieving and integrating diverse sets of motor information, such as where should one reach out or which arm is to be used. Next, based on the results of the studies on ideomotor apraxia, we have hypothesized that there are at least 2 distinct levels of neural representation (virtual level and physical level). We have reviewed the evidence supporting the operation of 2 distinct classes of neuronal activities corresponding to these 2 levels. In conclusion, we propose that the frontal cortex initially processes information across sensory and motor domains at the virtual level to generate information about a forthcoming motor action (virtual action plan) and that this information is subsequently transformed into a motor command, such as muscle activity or movement direction, for an actual body movement at the physical level (physical motor plan). This proposed framework may be useful for explaining the diverse clinical conditions caused by brain lesions as well as for clarifying the neural mechanisms underlying the integration of perception and action.

  13. CRMP-2 directly binds to cytoplasmic dynein and interferes with its activity Peer-reviewed

    Nariko Arimura, Atsushi Hattori, Toshihide Kimura, Shinichi Nakamuta, Yasuhiro Funahashi, Shinji Hirotsune, Kenya Furuta, Takashi Urano, Yoko Y. Toyoshima, Kozo Kaibuchi

    JOURNAL OF NEUROCHEMISTRY　111　(2)　380-390　2009/10

    DOI： 10.1111/j.1471-4159.2009.06317.x 　

    ISSN： 0022-3042

  14. TDP-43 Depletion Induces Neuronal Cell Damage through Dysregulation of Rho Family GTPases Peer-reviewed

    Yohei Iguchi, Masahisa Katsuno, Jun-ichi Niwa, Shin-ichi Yamada, Jun Sone, Masahiro Waza, Hiroaki Adachi, Fumiaki Tanaka, Koh-ichi Nagata, Nariko Arimura, Takashi Watanabe, Kozo Kaibuchi, Gen Sobue

    JOURNAL OF BIOLOGICAL CHEMISTRY　284　(33)　22059-22066　2009/08

    DOI： 10.1074/jbc.M109.012195 　

    ISSN： 0021-9258

    eISSN： 1083-351X

  15. 神経細胞における新規Slp1相互作用タンパク質の同定(Identification of Slp1-interacting proteins in neuron)

    船橋 靖広, 有村 奈利子, 中牟田 信一, 貝淵 弘三

    日本細胞生物学会大会講演要旨集　61回　191-191　2009/05

    Publisher: (一社)日本細胞生物学会

  16. Anterograde Transport of TrkB in Axons Is Mediated by Direct Interaction with Slp1 and Rab27 Peer-reviewed

    Nariko Arimura, Toshihide Kimura, Shinichi Nakamuta, Shinichiro Taya, Yasuhiro Funahashi, Atsushi Hattori, Akiko Shimada, Cine Menager, Saeko Kawabata, Kayo Fujii, Akihiro Iwamatsu, Rosalind A. Segal, Mitsunori Fukuda, Kozo Kaibuchi

    DEVELOPMENTAL CELL　16　(5)　675-686　2009/05

    DOI： 10.1016/j.devcel.2009.03.005 　

    ISSN： 1534-5807

  17. 細胞突起の形成と発達のメカニズム Rab27とSlp1によるTrkBの順行性輸送の制御(Developmental mechanisms of cellular processes Rab27 and Slp1 regulate anterograde transport of TrkB receptors in axons)

    有村 奈利子, 中牟田 信一, 船橋 靖広, 貝淵 弘三

    日本細胞生物学会大会講演要旨集　60回　75-75　2008/06

    Publisher: (一社)日本細胞生物学会

  18. Neurofibromatosis type 1 (NF1) tumor suppressor, neurofibromin, regulates the neuronal differentiation of PC12 cells via its associating protein, CRMP-2 Peer-reviewed

    Siriporn Patrakitkomjorn, Daiki Kobayashi, Takashi Morikawa, Masayo Morifuji Wilson, Nobuyuki Tsubota, Atsushi Irie, Tatsuya Ozawa, Masashi Aoki, Nariko Arimura, Kozo Kaibuchi, Hideyuki Saya, Norie Araki

    JOURNAL OF BIOLOGICAL CHEMISTRY　283　(14)　9399-9413　2008/04

    DOI： 10.1074/jbc.M708206200 　

    ISSN： 0021-9258

    eISSN： 1083-351X

  19. [Neuronal polarity]. Peer-reviewed

    Arimura N, Yoshimura T, Kaibuchi K

    Tanpakushitsu kakusan koso. Protein, nucleic acid, enzyme　53　(4 Suppl)　386-392　2008/03

    ISSN： 0039-9450

  20. CRMP-2とGSK-3は神経極性形成過程においてSlp 1とRab 27を介してTrkBの順行性輸送を制御する(CRMP-2 and GSK-3 regulate anterograde TrkB transport through Slp1 and Rab27 for neuronal polarization)

    有村 奈利子, 中牟田 信一, 島田 明子, 船橋 靖広, 貝淵 弘三

    日本生化学会大会・日本分子生物学会年会合同大会講演要旨集　80回・30回　1S16-2　2007/11

    Publisher: (公社)日本生化学会

  21. [Molecular mechanisms regulating neuronal polarity via phosphorylation signaling]. Peer-reviewed

    Yoshimura T, Arimura N, Hattori A, Kaibuchi K

    Tanpakushitsu kakusan koso. Protein, nucleic acid, enzyme　52　(7)　753-759　2007/06

    Publisher:

    ISSN： 0039-9450

  22. Rho-kinase modulates the function of STEF, a Rac GEF, through its phosphorylation Peer-reviewed

    Mikito Takefuji, Kazutaka Mori, Yasuhiro Morita, Nariko Arimura, Takashi Nishimura, Masanori Nakayama, Mikio Hoshino, Akihiro Iwamatsu, Toyoaki Murohara, Kozo Kaibuchi, Mutsuki Amano

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS　355　(3)　788-794　2007/04

    DOI： 10.1016/j.bbrc.2007.02.028 　

    ISSN： 0006-291X

  23. Neuronal polarity: From extracellular signals to intracellular mechanisms Peer-reviewed

    Nariko Arimura, Kozo Kaibuchi

    Nature Reviews Neuroscience　8　(3)　194-205　2007/03

    DOI： 10.1038/nrn2056 　

    ISSN： 1471-003X 1471-0048

  24. IQGAP3, a novel effector of Rac1 and Cdc42, regulates neurite outgrowth Peer-reviewed

    Shujie Wang, Takashi Watanabe, Jun Noritake, Masaki Fukata, Takeshi Yoshimura, Norimichi Itoh, Takumi Harada, Masato Nakagawa, Yoshiharu Matsuura, Nariko Arimura, Kozo Kaibuchi

    JOURNAL OF CELL SCIENCE　120　(4)　567-577　2007/02

    DOI： 10.1242/jcs.03356 　

    ISSN： 0021-9533

  25. Role of CRMP-2 in neuronal polarization Peer-reviewed

    Nariko Arimura, Takeshi Oshimura, Kozo Kaibuchi

    Intracellular Mechanisms for Neuritogenesis　239-252　2007

    Publisher: Springer US

    DOI： 10.1007/978-0-387-68561-8_11 　

  26. Signaling networks in neuronal polarization Peer-reviewed

    Takeshi Yoshimura, Nariko Arimura, Kozo Kaibuchi

    JOURNAL OF NEUROSCIENCE　26　(42)　10626-10630　2006/10

    DOI： 10.1523/JNEUROSCI.3824-06.2006 　

    ISSN： 0270-6474

  27. Myelin-associated glycoprotein inhibits microtubule assembly by a rho-kinase-dependent mechanism Peer-reviewed

    F Mimura, S Yamagishi, N Arimura, M Fujitani, T Kubo, K Kaibuchi, T Yamashita

    JOURNAL OF BIOLOGICAL CHEMISTRY　281　(23)　15970-15979　2006/06

    DOI： 10.1074/jbc.M510934200 　

    ISSN： 0021-9258

  28. Vimentin-Ser82 as a memory phosphorylation site in astrocytes Peer-reviewed

    T Oguri, A Inoko, H Shima, Izawa, I, N Arimura, T Yamaguchi, N Inagaki, K Kaibuchi, K Kikuchi, M Inagaki

    GENES TO CELLS　11　(5)　531-540　2006/05

    DOI： 10.1111/j.1365-2443.2006.00961.x 　

    ISSN： 1356-9597

  29. [Neuronal polarity]. Peer-reviewed

    Arimura N, Yoshimura T, Kaibuchi K

    Tanpakushitsu kakusan koso. Protein, nucleic acid, enzyme　51　(6 Suppl)　789-795　2006/05

    ISSN： 0039-9450

  30. Ras regulates neuronal polarity via the PI3-kinase/Akt/GSK-3 beta/CRMP-2 pathway Peer-reviewed

    T Yoshimura, N Arimura, Y Kawano, S Kawabata, SJ Wang, K Kaibuchi

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS　340　(1)　62-68　2006/02

    DOI： 10.1016/j.bbrc.2005.11.147 　

    ISSN： 0006-291X

  31. Molecular mechanisms of axon specification and neuronal disorders Peer-reviewed

    Takeshi Yoshimura, Nariko Arimura, Kozo Kaibuchi

    INTEGRATED MOLECULAR MEDICINE FOR NEURONAL AND NEOPLASTIC DISORDERS　1086　116-125　2006

    DOI： 10.1196/annals.1377.013 　

    ISSN： 0077-8923

  32. Key regulators in neuronal polarity Peer-reviewed

    N Arimura, K Kaibuchi

    NEURON　48　(6)　881-884　2005/12

    DOI： 10.1016/j.neuron.2005.11.007 　

    ISSN： 0896-6273

    eISSN： 1097-4199

  33. Phosphorylation by Rho kinase regulates CRMP-2 activity in growth cones Peer-reviewed

    N Arimura, C Menager, Y Kawano, T Yoshimura, S Kawabata, A Hattori, Y Fukata, M Amano, Y Goshima, M Inagaki, N Morone, J Usukura, K Kaibuchi

    MOLECULAR AND CELLULAR BIOLOGY　25　(22)　9973-9984　2005/11

    DOI： 10.1128/MCB.25.22.9973-9984.2005 　

    ISSN： 0270-7306

  34. Molecular mechanisms of neuronal polarity Peer-reviewed

    Takeshi Yoshimura, Yoji Kawano, Nariko Arimura, Saeko Kawabata, Kozo Kaibuchi

    Japanese Journal of Neuropsychopharmacology　25　(4)　169-174　2005/08

    ISSN： 1340-2544

  35. Tubulin and CRMP-2 complex is transported via Kinesin-1

    Kimura T, Arimura N, Fukata Y, Watanabe H, Iwamatsu A, Kaibuchi K

    Journal of Neurochemistry　93　1371-1382　2005/06

    DOI： 10.1111/j.1471-4159.2005.03063.x 　

    ISSN： 0022-3042

  36. Edg8/S1P5: An oligodendroglial receptor with dual function on process retraction and cell survival Peer-reviewed

    C. Jaillard, S. Harrison, B. Stankoff, M. S. Aigrot, A. R. Calver, G. Duddy, F. S. Walsh, M. N. Pangalos, N. Arimura, K. Kaibuchi, B. Zalc, C. Lubetzki

    Journal of Neuroscience　25　(6)　1459-1469　2005/02/09

    DOI： 10.1523/JNEUROSCI.4645-04.2005 　

    ISSN： 0270-6474

  37. GSK-3 beta regulates phosphorylation of CRMP-2 and neuronal polarity Peer-reviewed

    T Yoshimura, Y Kawano, N Arimura, S Kawabata, A Kikuchi, K Kaibuchi

    CELL　120　(1)　137-149　2005/01

    DOI： 10.1016/j.cell.2004.11.012 　

    ISSN： 0092-8674

  38. PIP3 is involved in neuronal polarization and axon formation Peer-reviewed

    C Menager, N Arimura, Y Fukata, K Kaibuchi

    JOURNAL OF NEUROCHEMISTRY　89　(1)　109-118　2004/04

    DOI： 10.1046/j.1471-4159.2004.02302.x 　

    ISSN： 0022-3042

  39. Role of CRMP-2 in neuronal polarity Peer-reviewed

    N Arimura, C Menager, Y Fukata, K Kaibuchi

    JOURNAL OF NEUROBIOLOGY　58　(1)　34-47　2004/01

    DOI： 10.1002/neu.10269 　

    ISSN： 0022-3034

  40. CRMP-2 induces axons in cultured hippocampal neurons

    INAGAKI N

    Nature Neurosci　4　(8)　781-782-782　2001

  41. Phosphorylation of collapsin response mediator protein-2 by Rho-kinase - Evidence for two separate signaling pathways for growth cone collapse

    N Arimura, N Inagaki, K Chihara, C Menager, N Nakamura, M Amano, A Iwamatsu, Y Goshima, K Kaibuchi

    JOURNAL OF BIOLOGICAL CHEMISTRY　275　(31)　23973-23980　2000/08

    DOI： 10.1074/jbc.M001032200 　

    ISSN： 0021-9258

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Misc. 39

  1. Chapter 3: Adhesion molecules in astrocytes

    Nariko Arimura

    Astrocytes Wiring the Brain, 2nd edition　2025/11

  2. 神経膜分子DSCAMによるグルタミン酸除去制御

    有村奈利子, 出羽健一, 出羽健一, 星野幹雄

    日本生化学会大会(Web)　94th　2021

  3. DSCAMによるRapGEF2/Rap1とN-Cadherinの抑制が神経細胞の脱上皮化と細胞移動を制御する

    有村奈利子, 岡田茉子, 岡田茉子, 田谷真一郎, 出羽健一, 出羽健一, 植竹寛倫, 西岡朋生, 井上由紀子, 井上高良, 貝淵弘三, 星野幹雄

    日本分子生物学会年会プログラム・要旨集(Web)　42nd　2019

  4. 小脳興奮性シナプス形成におけるダウン症関連分子の機能解析

    出羽健一, 出羽健一, 有村奈利子, 田谷真一郎, 境和久, 一戸紀孝, 宮崎大輔, 山崎美和子, 渡辺雅彦, 井上由紀子, 小泉修一, 星野幹雄

    日本分子生物学会年会プログラム・要旨集(Web)　42nd　2019

  5. 中脳神経細胞の脳室面離脱におけるダウン症関連因子による制御機構の解析

    有村奈利子, 出羽健一, 出羽健一, 岡田茉子, 岡田茉子, 柳川右千夫, 田谷真一郎, 星野幹雄

    日本分子生物学会年会プログラム・要旨集(Web)　41st　2018

  6. 小脳興奮性シナプスにおけるダウン症関連分子の機能解析

    出羽 健一, 有村 奈利子, 田谷 真一郎, 堺 和久, 小泉 修一, 星野 幹雄

    生命科学系学会合同年次大会　2017年度　[1P-1300]　2017/12

    Publisher: 生命科学系学会合同年次大会運営事務局

  7. 小脳興奮性シナプスにおけるダウン症関連分子の機能解析

    出羽 健一, 有村 奈利子, 田谷 真一郎, 堺 和久, 小泉 修一, 星野 幹雄

    生命科学系学会合同年次大会　2017年度　[1P-1300]　2017/12

    Publisher: 生命科学系学会合同年次大会運営事務局

  8. 中脳神経細胞の細胞移動におけるダウン症関連因子の機能解析

    有村 奈利子, 出羽 健一, 岡田 茉子, 柳川 右千夫, 田谷 真一郎, 星野 幹雄

    生命科学系学会合同年次大会　2017年度　[3P-1180(4P1T08　2017/12

    Publisher: 生命科学系学会合同年次大会運営事務局

  9. 中脳神経細胞の細胞移動におけるダウン症関連因子の機能解析

    有村 奈利子, 出羽 健一, 岡田 茉子, 柳川 右千夫, 田谷 真一郎, 星野 幹雄

    生命科学系学会合同年次大会　2017年度　[4P1T08-13(3P　2017/12

    Publisher: 生命科学系学会合同年次大会運営事務局

  10. 行動ゴール達成過程における複数脳領域の関与の比較

    81st　600　2017/08

  11. 小脳興奮性シナプス形成におけるダウン症関連分子の機能解析

    出羽健一, 有村奈利子, 田谷真一郎, 小泉修一, 星野幹雄

    日本生物学的精神医学会(Web)　38th　2016

  12. ダウン症関連分子による神経細胞移動の分子機構の解明

    田谷 真一郎, 有村 奈利子, 出羽 健一, 早瀬 ヨネ子, 柳川 右千夫, 星野 幹雄

    日本生化学会大会・日本分子生物学会年会合同大会講演要旨集　88回・38回　[2P1318]-[2P1318]　2015/12

    Publisher: (公社)日本生化学会

  13. 生後小脳におけるダウン症関連遺伝子の解析

    出羽 健一, 田谷 真一郎, 有村 奈利子, 星野 幹雄, 小泉 修一

    日本生化学会大会・日本分子生物学会年会合同大会講演要旨集　88回・38回　[2P1319]-[2P1319]　2015/12

    Publisher: (公社)日本生化学会

  14. Differential distribution of activities reflecting planning, preparation, and execution of action in six motor areas of the frontal lobe

    Yoshihisa Nakayama, Tomoko Yamagata, Nariko Arimura, Jun Tanji, Eiji Hoshi

    NEUROSCIENCE RESEARCH　71　E347-E347　2011

    DOI： 10.1016/j.neures.2011.07.1521 　

    ISSN： 0168-0102

  15. A comparison of neuronal activity of globus pallidus and premotor cortex in retrieving a virtual action plan instructed by a visual object and in developing a physical motor plan

    Nariko Arimura, Yoshihisa Nakayama, Tomoko Yamagata, Jun Tanji, Eiji Hoshi

    NEUROSCIENCE RESEARCH　71　E346-E346　2011

    DOI： 10.1016/j.neures.2011.07.1516 　

    ISSN： 0168-0102

  16. 認知と運動の統合過程を支える神経基盤

    星 英司, 中山 義久, 山形 朋子, 佐賀 洋介, 橋本 雅史, 有村 奈利子, 丹治 順

    BRAIN and NERVE: 神経研究の進歩　63　(1)　59-68　2011/01

    Publisher: (株)医学書院

    ISSN： 1881-6096

  17. 【大脳機能局在はここまで分かった】 前頭葉 補足運動野と前補足運動野

    丹治 順, 中山 義久, 山形 朋子, 佐賀 洋介, 橋本 雅史, 有村 奈利子, 星 英司

    Clinical Neuroscience　28　(10)　1121-1124　2010/10

    Publisher: (株)中外医学社

    ISSN： 0289-0585

  18. 運動実行に関わる神経細胞活動の前頭葉6領域間の比較(Comparison of movement-related neuronal activity recorded from six different areas in the frontal cortex of macaques)

    中山 義久, 山形 朋子, 有村 奈利子, 丹治 順, 星 英司

    神経化学　49　(2-3)　637-637　2010/08

    Publisher: 日本神経化学会

    ISSN： 0037-3796

  19. 行動の抽象表現に基づく運動計画における大脳基底核と前頭前野の関与(Involvement of the basal ganglia and the frontal cortex in action planning as mediated by the abstract representation of action)

    有村 奈利子, 中山 義久, 山形 朋子, 佐賀 洋介, 丹治 順, 星 英司

    神経化学　49　(2-3)　637-637　2010/08

    Publisher: 日本神経化学会

    ISSN： 0037-3796

  20. Comparison of movement-related neuronal activity recorded from six different areas in the frontal cortex of macaques

    Yoshihisa Nakayama, Tomoko Yamagata, Nariko Arimura, Jun Tanji, Eiji Hoshi

    NEUROSCIENCE RESEARCH　68　E265-E265　2010

    DOI： 10.1016/j.neures.2010.07.1175 　

    ISSN： 0168-0102

  21. Involvement of the basal ganglia and the frontal cortex in action planning as mediated by the abstract representation of action

    Nariko Arimura, Yoshihisa Nakayama, Tomoko Yamagata, Yosuke Saga, Jun Tanji, Eiji Hoshi

    NEUROSCIENCE RESEARCH　68　E265-E265　2010

    DOI： 10.1016/j.neures.2010.07.1177 　

    ISSN： 0168-0102

  22. Identification of PI 3-kinase as an Slp1-interacting protein by proteomic analysis

    Yasuhiro Funahashi, Nariko Arimura, Shinichi Nakamuta, Kozo Kaibuchi

    NEUROSCIENCE RESEARCH　65　S199-S199　2009

    DOI： 10.1016/j.neures.2009.09.1089 　

    ISSN： 0168-0102

  23. Involvement of subareas within the dorsal premotor area (PMd) in a conceptually demanding visuomotor task

    Yoshihisa Nakayama, Nariko Arimura, Tomoko Yamagata, Jun Tanji, Eiji Hoshi

    NEUROSCIENCE RESEARCH　65　S168-S168　2009

    DOI： 10.1016/j.neures.2009.09.877 　

    ISSN： 0168-0102

  24. 神経細胞の極性制御機構

    有村 奈利子, 吉村 武, 貝淵 弘三

    神経の分化，回路形成，機能発現、蛋白質 核酸 酵素　53　(4)　386-392　2008/03

  25. Regulation machinery of neurite extention by Rho-kinase and GSK-3β inhibitors

    ARIMURA Nariko, YOSHIMURA Takeshi, KAIBUCHI Kozo

    18　(2)　107-110　2007/12/01

    ISSN： 0917-6772

  26. Rho-kinaseによるRacGEF(STEF)のリン酸化

    森 和孝, 竹藤 幹人, 有村 奈利子, 中山 雅敬, 室原 豊明, 貝淵 弘三, 天野 睦紀

    日本薬理学雑誌　130　(3)　18P-18P　2007/09

    Publisher: (公社)日本薬理学会

    ISSN： 0015-5691

    eISSN： 1347-8397

  27. Neuronal polarity and axonal vesicle transport

    K. Kaibuchi, N. Arimura

    JOURNAL OF NEUROCHEMISTRY　102　168-168　2007/08

    ISSN： 0022-3042

  28. リン酸化シグナルが制御する神経細胞の極性形成メカニズム

    吉村 武, 有村 奈利子, 服部 敦志, 貝淵 弘三

    蛋白質 核酸 酵素　52　(7)　753-759　2007/06

  29. Neuronal polarity: from extracellular signals to intracellular mechanisms

    Nariko Arimura, Kozo Kaibuchi

    NATURE REVIEWS NEUROSCIENCE　8　(3)　194-205　2007/03

    DOI： 10.1038/nrn2056 　

    ISSN： 1471-0048

  30. CRMP-2, Slp1 and Rab278 mediate anterograde transport of TrkB

    Nariko Arimura, Akiko Shimada, Kozo Kaibuchi

    NEUROSCIENCE RESEARCH　58　S39-S39　2007

    ISSN： 0168-0102

  31. 神経細胞の極性形成に関与する分子の網羅的解析

    吉村 武, 有村 奈利子, 貝淵 弘三

    細胞工学　25　(6)　636-641　2006/06

  32. 神経極性

    有村 奈利子, 吉村 武, 貝淵 弘三

    細胞骨格と接着、蛋白質 核酸 酵素　51　(6)　789-795　2006/05

  33. 神経再生の新たな視点を求めて、特に、制御機構について Rho-kinaseおよびGSK-3betaと軸索伸長

    有村 奈利子, 貝淵 弘三

    解剖学雑誌　81　(Suppl.)　100-100　2006/03

    Publisher: (一社)日本解剖学会

    ISSN： 0022-7722

  34. Role of a novel collapsin response mediator protein-2 interacting molecule, synaptotagmin-like protein in hippocampal neuron

    Nariko Arimura, Saeko Kawabata, Atsushi Hattori, Kozo Kaibuchi

    NEUROSCIENCE RESEARCH　55　S56-S56　2006

    ISSN： 0168-0102

  35. 神経細胞の極性を司る分子機構

    吉村 武, 河野 洋治, 有村 奈利子, 川端 紗枝子, 貝淵 弘三

    日本神経精神薬理学雑誌　25　(4)　169-174　2005/08

  36. リン酸化が制御する神経細胞極性化の新規メカニズム

    有村 奈利子, 吉村 武, 川端 紗枝子, 服部 敦志, 貝淵 弘三

    実験医学　23　(13)　2012-2016　2005/08

  37. 神経細胞の極性を制御する分子機構

    吉村 武, 河野 洋治, 有村 奈利子, 川端 紗枝子, 貝淵 弘三

    細胞工学　24　(3)　231-235　2005/03

  38. CRMP-2による神経極性形成の制御機構

    有村奈利子, 稲垣直之, 貝淵弘三

    実験医学　19　2309-2311　2001

  39. Activation of Ca2+/calmodulin-dependent protein kinase II within post-synaptic dendritic spines of cultured hippocampal neurons

    N Inagaki, M Nishizawa, N Arimura, H Yamamoto, Y Takeuchi, E Miyamoto, K Kaibuchi, M Inagaki

    JOURNAL OF BIOLOGICAL CHEMISTRY　275　(35)　27165-27171　2000/09

    DOI： 10.1074/jbc.M003751200 　

    ISSN： 0021-9258

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Presentations 29

  1. Investigating the cognitive and molecular impact of Down Syndrome bone marrow transplantation Invited

    Nariko Arimura

    The 15 th BRI International Symposium (Brain Research Institute, Niigata University)　2025/03/15

  2. Network formation induced by membrane molecular interactions between neurons and glial cells Invited

    Nariko Arimura

    The 98th Annual Meeting of the Japanese Pharmacological Society　2025/03/11

  3. From cells to the brain: A multifaceted approach to understanding brain function Invited

    Nariko Arimura

    The 42nd Molecular Circuit Seminar at the National Institute of Neuroscience (National Center of Neurology and Psychiatry)　2025/03/05

  4. DSCAM as a Key Regulator of Neural Delamination and Synaptic Connectivity Invited

    Nariko Arimura

    Adaptive circuit census International Symposium 2025 (BSI, Riken)　2025/01/24

  5. Diverse functions of the neuronal membrane molecule DSCAM during development Invited

    Nariko Arimura

    47th Annual Meeting of the Molecular Biology Society　2024/11/22

  6. Multifaceted Functions of the Adhesion Molecule DSCAM in Neural Development Invited

    Nariko Arimura

    Neuro2024　2024/07/25

  7. From Marrow to Memory: Tracing Dementia Onset using Down Syndrome Model Mice

    Nariko Arimura

    The 21st Core to Core Program Symposium, IRCMS, Kumamoto University　2024/02/20

  8. 骨髄移植による認知症発症メカニズムの解析

    有村 奈利子 (座長)

    第97回日本薬理学会年会　2023/12/15

  9. 造血幹細胞を介した認知症発症基盤の解明 Invited

    有村奈利子

    第46回日本神経組織培養研究会　2023/12/02

  10. Bone-marrow-derived cells in trisomy are implicated in dementia

    2023/08/01

  11. Analysis of the mechanism of cognitive function modification by bone marrow transplantation

    2023/07/22

  12. 神経接着分子DSCAMによるグリア細胞膜分子GLASTの機能制御 Invited

    有村奈利子

    第128回日本解剖学会総会　2023/03/18

  13. 認知症を引き起こす新たな血液由来成分の探索 Invited

    有村奈利子

    第７回医薬品開発研究センターシンポジウム　2023/03/07

  14. Functional analysis of Down syndrome-related factor DSCAM at cerebellar synapses

    Nariko Arimura

    2022/11/11

  15. The Multiple Function of Neural Transmembrane Protein DSCAM: Neuronal Migration and Synapse Formation Invited

    Nariko Arimura

    2022/11/08

  16. Molecular Interactions between Astrocytes and Purkinje Cells: Regulation of Synaptic Localization of GLAST and Synaptogenesis

    Nariko Arimura

    2021/12/01

  17. 小脳プルキンエ細胞上のDSCAM によるグリア細胞上のGLASTの局在とシナプス形成制御 Invited

    有村 奈利子

    第43回神経組織培養研究会　2021/11/07

  18. Regulation of Glutamate Uptake by Neuronal Transmembrane Protein DSCAM

    Nariko Arimura

    The 94th Annual Meeting of the Japanese Biochemical Society　2021/11/04

  19. Purkinje cell DSCAM regulates Bergmann glial GLAST localization near synaptic cleft and cerebellar synapse development

    Nariko Arimura

    The 64th Annual Meeting of the Japanese Society for Neurochemistry　2021/10/01

  20. The role of DSCAM in the cerebellar synaptogenesis

    Nariko Arimura

    2021/07/29

  21. DSCAM Regulates Neuronal Delamination Through Suppression of RapGEF2/Rap1 and N-Cadherin

    Nariko Arimura

    MBSJ2020　2020/12/04

  22. Regulation of Neuronal Delamination by DSCAM and its signaling molecules

    Nariko Arimura

    The 63rd Annual Meeting of the Japanese Society for Neurochemistry　2020/09/11

  23. DSCAM-Mediated Suppression of RapGEF2/Rap1 and N-Cadherin Regulates Neuronal Delamination and Migration

    Nariko Arimura, Mako Okada, Shin-ichiro Taya, Ken-ichi Dewa, Hirotomo Uetake, Tomoki Nishioka, Yukiko U. Inoue, Takayoshi Inoue, Kozo Kaibuch, Mikio Hoshino

    MBSJ2019　2019/12/04

  24. The functional analysis of a down syndrome-associated gene in neuronal migration of midbrain neurons. International-presentation

    Arimura N, Dewa K, Okada M, Yanagawa Y, Taya S, Hoshino M

    The 12 th annual meeting for Japanese Developmental Neuroscientists　2019/03

  25. The functional analysis of a down syndrome-associated gene in neuronal migration of midbrain neurons

    Arimura N, Dewa K, Okada M, Yanagawa Y, Taya S, Hoshino M

    ConBio2017　2017/12

  26. 新規Collapsin response mediator protein-2結合蛋白質synaptotagmin-like proteinの海馬神経細胞における機能解析

    有村奈利子, 川端紗枝子, 服部敦志, 貝淵弘三

    第２９回日本神経科学大会　2006/06

  27. Key regulators in neuronal polarity. International-presentation

    Arimura N, Yoshimura T, Kaibuchi K

    IUBMB2006　2006/06

  28. The regulation of neuronal polarization by CRMP-2. International-presentation

    Arimura N, Yoshimura T, Kaibuchi K

    Neuroscience2005　2005/11

  29. Soluble form of tubulin is transported as a complex with CRMP-2 by conventional kinesin in growing axon. International-presentation

    Arimura N, Kimura T, Fukata Y, Watanabe H, Iwamatsu A, Kaibuchi K

    Federation of European Neuroscience societies (FENS)　2004/07

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Research Projects 17

  1. Prevailing over Down Syndrome using Non-Genome Altering Mosaic-Inducing Methods

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research

    Category: Grant-in-Aid for Scientific Research (B)

    Institution: Mie University

    2025/04/01 - 2029/03/31

  2. Analysis of plasma components involved in the development of dementia and development of transplantation therapy

    2024/09 - 2027/03

  3. Elucidation of the mechanism of dementia pathogenesis via hematopoietic stem cells

    Nariko Arimura

    Offer Organization: Japan Society for the Promotion of Science

    System: KAKENHI

    Institution: Tohoku University

    2024/04 - 2027/03

  4. 細胞間相互作用を介したグルタミン酸トランスポーターのシナプス局在制御機構

    有村奈利子

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業 基盤研究(C)

    Institution: 国立研究開発法人国立精神・神経医療研究センター

    2021/04 - 2024/03

  5. Ｄｓｃａｍによる神経細胞移動制御機構の解析

    有村 奈利子

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業 特別研究員奨励費

    Category: 特別研究員奨励費

    Institution: 国立研究開発法人国立精神・神経医療研究センター

    2017/04 - 2021/03

    More details Close

    これまでの解析で、中脳神経細胞は DSCAM/RapGEF2/Rap1という共通の分子カスケードを細胞移動開始に必要とすることを明らかにしてきた。本研究課題では、DSCAMによる、脳室面からの脱上皮化がどのような分子機序によりなされるかについて解析をおこなった。これまでの研究において、中脳神経細胞が生み出される胎生期の半ばE13.5において、脳室面離脱時に形成される神経細胞の形態変化および終足の退縮が、Dscamにより制御されることを新規に明らかにした。またDSCAMの機能の下流で、RapGEF2/Rap1が不活化し、それによりN-cadherinの不安定化すること、接着面の N-cadherinが減少すること等が、神経細胞の脳室面離脱に必要であることが明らかとなった。これらの結果については、現在論文を投稿し、リバイス中である。また、RapGEF2はRapGEF6と重複する機能を有することが示唆されていたが、中脳神経細胞では、その局在を異にしており、機能的差異があることが新たに示唆された。さらに、RapGEF2とDSCAMは、膜分子の裏打ちとして機能するMAGI1と相互作用して３者複合体を形成し、MAGIの結合がRapGEF2の活性制御に重要であることを見出している。今後は、今後はDSCAMの神経細胞移動時の接着制御がどのような分子基盤により制御されているかを検証してゆく。

  6. Elucidation of novel patterns of neuronal development and migration using the midbrain as a model system

    Arimura Nariko

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research

    Category: Grant-in-Aid for Scientific Research (C)

    Institution: National Center of Neurology and Psychiatry

    2017/04 - 2021/03

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    The midbrain is a critical region that controls cognitive, emotional, and motor functions. However, the developmental mechanisms of neurons in the midbrain are still unclear. Many CNS cells undergo cell migration after differentiation in the ventricular surface and other areas since their product's location differs from the site where they are located and function. This study aims to elucidate the molecular mechanisms of neuronal migration using the midbrain, which develops during the earliest stages of evolution, as a model system. We have summarized the results of our studies on the migration patterns of mesencephalic neurons and elucidated the molecular mechanisms that control the de-epithelialization of the ventricular surface immediately after differentiation, which occurs at the beginning of neuronal migration by using tissue staining and time-lapse techniques. These results were summarized in a paper and published.

  7. 光刺激操作を用いた内発性動作における基底核—運動前野ネットワークの機能解析 Competitive

    有村 奈利子

    Offer Organization: 日本学術振興会 科学研究費助成事業

    System: 基盤研究(C)

    2012 - 2015

  8. MOLECULAR MECHANISMS UNDERLYING CELL POLARIZATION IN MIGRATING CELLS AND NEURONS

    KAIBUCHI Kozo, AMANO Mutsuki, WATANABE Takashi, MORI Daisuke, NISHIOKA Tomoki, TSUBOI Daisuke, ARIMURA Nariko

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research

    Category: Grant-in-Aid for Scientific Research (S)

    Institution: Nagoya University

    2008 - 2012

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    In response to extracellular and intracellular signals, cell exhibits a polarized morphology with adhering neighboring cells and extracellular matrix. Cell polarization is a fundamental process that makes cells enable to exert specific physiological roles in tissues. The understanding for the molecular mechanisms by which cell polarization isregulated had remained largely unknown. Our researches revealed signaling networks for cellular polarization and its maintenance in migrating cells and neurons.

  9. The study of molecular basis underlying the motor control in the basal ganglia. Competitive

    ARIMURA Nariko

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research

    Category: Grant-in-Aid for Young Scientists (B)

    Institution: Tamagawa University

    2010 - 2011

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    It is essential to understand the property of neural population consisting of the brain and the constitution of neural network in familiarization with the variety of brain function and the nerve disease. However, in the higher brain function including the mood and motor control, it still lacks the global analysis to reveal what kinds of neuronal populations showing the unique gene expression patterns interplay with several neuronal populations using what molecular mechanisms, and which neural function was generated. In this study, I analyzed the gene expression pattern in the globus pallidus, as an output device of the basal ganglia mediated mood and motor control.

  10. The functional analysis of key molecule in axon formation, CRMP-2

    ARIMURA Nariko

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research

    Category: Grant-in-Aid for Young Scientists (B)

    Institution: Tamagawa University

    2008 - 2009

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    The brain consists of the remarkably fine neural circuits. This circuits are made of axons, and CRMP-2 previously had been identified as a key molecule in axon formation. I analyzed the functional meaning of CRMP-2 in axon formation, and obtained the following results : 1) CRMP-2 regulates anterograde TrkB transport in axon through the association with Slp1 and Rab27. 2) CRMP-2 binds directly to cytoplasmic dynein, a motor protein of retrograde transport, and negatively regulates its function. These results suggest that CRMP-2 play a role in axon formation through regulating the molecular transport in axon.

  11. CFTR-SLC26輸送体複合体のイオン輸送機能における低分子量G蛋白質の役割

    洪 繁, 石黒 洋, 山本 明子, 有村 奈利子, 相馬 義郎, 後藤 秀実

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業

    Category: 特定領域研究

    Institution: 名古屋大学

    2008 - 2009

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    膵導管細胞は全身の上皮膜中で、最も高い濃度の重炭酸イオン(HCO_3^-:～125mM)を含むアルカリを分泌する。これまでの我々自身の研究で、このアルカリ分泌には膵導管細胞管腔膜に発現するCFTR(Cystic Fibrosis Transmembrane conductance Regulator)クロライド(Cl^-)チャネルとSLC(Solute Carrier)26輸送体の働きが重要であることを明らかにしてきた。特にSLC26陰イオン交換輸送体は、CFTRが導管細胞管腔内に分泌したCl^-を吸収し、交換にHCO_3^-を分泌することで膵液中の高いHCO_3^-濃度維持に働いている。本研究では、膵導管細胞における重炭酸イオン輸送調節機構を明らかにするために、SLC26輸送体の細胞内STAS(Sulfate Transporter Anti-Sigma factor antagonist)ドメインに結合する新規蛋白の同定を試みた。GSTタグを付加したヒトSLC26A6 STASドメインをベイトにして、ヒト膵癌細胞株Capan-1の細胞溶解液中に存在するSTAS結合新規蛋白をpull down法で同定した。その結果、guanine nucleotide exchange factor(GEF)ドメインを持つGEF蛋白及びGTPase Activating Protein(GAP)を持つGAP蛋白が同定された。これらの蛋白はA6-STASドメインと結合することが免疫沈降法で確認され、またこれらの蛋白と全長のSLC26A6をCOS7細胞に共発現させるとGEF蛋白はSLC26A6の陰イオン交換輸送活性を活性化し、反対にGAP蛋白はSLC26A6の陰イオン交換輸送活性を抑制することが確認された。SLC26輸送体ファミリー蛋白は、すべてのisoformが細胞内STASドメインを有しているが、SLC26輸送体はこれらのGEFやGAP蛋白により正又は負に活性制御を受けている可能性が明らかとなった。

  12. Molecular mechanism underlying neuronal polarity

    KAIBUCHI Kozo, NARIKO Arimura, DAISUKE Mori, TOMOKI Nishioka

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research

    Category: Grant-in-Aid for Scientific Research on Priority Areas

    Institution: Nagoya University

    2005 - 2009

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    Our project aimed at examining the molecular mechanisms underlying establishment and maintenance of neuronal polarity. We found that GSK-3β regulates neuronal polarity through the phosphorylation of CRMP-2. CRMP-2 complex directly links Kinesin-1 motor, and this association is required for the anterograde transport of signaling molecules and polarity related proteins-containing vesicles.

  13. CRMP-2 による神経細胞の極性形成機構の解明 Competitive

    有村 奈利子

    Offer Organization: 日本学術振興会

    System: 若手研究(B)

    Category: 若手研究(B)

    Institution: 名古屋大学

    2006 - 2007

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    脳神経系は極めて精巧な神経回路網を有する。このような神経回路網の形成には、軸索と樹状突起という2つの異なる神経突起が複雑にシナプスを形成することで機能している。しかしながらこれらの突起の形成メカニズムについては不明な点が多い。以前私はcollapsin response mediator protein-2(CRMP-2)が軸索の伸長や退縮に関与することを明らかにしてきた。さらに近年、CRMP-2が軸索/樹状突起の運命決定を担い、極性形成や軸索伸長に重要な役割を果たすことが提唱されている。最近私はCRMP-2がsynaptotagmin-like protein 1 (Slp1)と結合することを明らかにした。Slp1はRab27と結合し、小胞輸送に関与することが示唆されている。我々はCRMP-2が、Slp/Rab27Bと複合体を形成することを明らかにした。Slp1は神経成長因子の受容体であるTrkBと共局在し、Slp1/Rab27Bと複合体を形成することが示唆された。このTrkB-Slp1/Rab27の結合は、TrkBの細胞内領域とSlp1のC末端側との直接結合を介していた。また、TrkBの細胞内領域と相同性のある一部の成長因子受容体もSlp1と結合することを見出した。免疫沈降実験の結果、Slp1がCRMP-2を介して、KIF5とKLCと結合していることが示された。タイムラプス法でTrkB-mCherryの動きを確認すると、軸索において順行性、逆行性の両方の動きが観察された。また、Slp1やCRMP-2,KLCの機能をsiRNA干渉法にて阻害すると、TrkB-mCherryの順行性輸送が障害された。以上の結果は、極性形成を制御するCRMP-2は様々な分子と相互作用し、積み荷受容体として細胞内輸送を制御している事が明らかとなった。

  14. Molecular mechanism underlying cell polarity and cell migration

    KAIBUCHI Kozo, USUKURA Jiro, KURODA Shinya, AMANO Mutsuki, TAYA Shinichiro, ARIMURA Nariko

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research

    Category: Grant-in-Aid for Creative Scientific Research

    Institution: Nagoya University

    2003 - 2007

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    Cell polarization is an essential step for cellular functions, but the underlying mechanisms to establish and maintain cell polarity are not fully understood. We tried to clarify the signal transduction mechanisms controlling cell polarization by the use of cell migration and neuronal axon/dendrite determination as model systems. 1. Identification of extracellular signals modulating neuronal polarity and following signaling pathways. Extracellular signals such as laminin induced the production of PIP3, inactivation of GSK-3β, and resultant activation of CRMP-2. Active CRMP-2 bound to tubulin, Sra-1, and Numb, and regulated tubulin polymerization, actin remodeling, and L1 endocytosis at growth cone, which contributed to the axon elongation and neuronal axon/dendrite determination. In addition, Par complex composed of Par-3, Pare and aPKC modulated the Rac activity through Rac GEF (Tiam1/Tiam2) to establish neuronal polarity and front-rear polarity of migrating cells. 2. Analysis of signaling pathways underlying cell migration During establishment and maintenance of front-rear polarity in cell migration, Rac/IAGAP1 regulated dynamics of both actin and microtubules through APC/CLIP-170. Rho/Rho-kinase inhibited Par complex formation and adjusted the Rac activity properly both at the front and rear. 3. Role of molecular and vesicular traffic in cell polarization and migration CRMP-2 interacted with tubulin, Sra-1 and Slp1/TrkB, and transported them to the tip of axon as a “cargo receptor". Numb regulated integrin endocytosis at the front of migrating cell, which is supposed to be necessary for directional migration. 4. Analysis of signal networks by computer simulation The computational model for endothelial cell contraction (activation of myosin) suggested the existence of unidentified pathway for sustained cell contraction in silico, and the novel pathway mediated by iPLA2 was identified in vivo. The computational model for establishment of front-rear polarity of migrating cells by Rho family GTPases was developed.

  15. 神経回路網形成におけるCRMP-2 の機能解析 Competitive

    有村 奈利子

    Offer Organization: 日本学術振興会

    System: 10) 特別研究員奨励費

    Category: 特別研究員奨励費

    2004 - 2005

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    脳神経系は極めて精巧な神経回路網を有する。このような神経回路網の形成には、軸索と樹状突起という2つの異なる神経突起が複雑にシナプスを形成することで形成、機能している。しかしながらこれらの突起の形成メカニズムについては不明な点が多い。 以前私はcollapsin response mediator protein-2(CRMP-2)が軸索の伸長や退縮に関与することを明らかにしてきた。さらに近年、CRMP-2が軸索/樹状突起の運命決定を担い、極性形成や軸索伸長に重要な役割を果たすことが提唱されている。最近我々はCRMP-2が低分子量G蛋白質Rhoの標的蛋白質Rhoキナーゼによってリン酸化されると、チューブリンやNumbとの結合能を失うことを明らかにした。しかしActinとの結合にはリン酸化による影響は見られなかった。反発性軸索ガイダンス因子であるephrin-A5刺激による成長円錐の退縮時に、CRMP-2のリン酸化レベルの上昇が見られた。これらの結果は、成長円錐の退縮時にRhoキナーゼがCRMP-2をリン酸化し、CRMP-2とその結合分子との相互作用を制御することによりCRMP-2の機能を阻害していることを示唆している。CRMP-2はGSK-3βによってもリン酸化される。Rhoキナーゼと同様に、GSK-3βによるCRMP-2のリン酸化によってCRMP-2はチューブリンと結合しなくなり、不活性化されることも見出した。さらに、GSK-3βの上流にRasが存在していることが明らかとなった。Rasが活性化するとPI3-kinase/Akt/GSK-3βを介してCRMP-2のリン酸化を抑制し、従って軸索形成を促進することが明らかとなった。以上の結果から、極性形成を制御するCRMP-2は様々な分子と相互作用し、細胞外シグナル依存的にリン酸化され、その活性が制御されることが明らかとなった。

  16. Rho キナーゼとCRMP-2 による神経回路網形成機構の解明 Competitive

    有村 奈利子

    Offer Organization: 日本学術振興会

    System: 特別研究員奨励費

    Category: 特別研究員奨励費

    Institution: 名古屋大学

    2001 - 2003

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    脳神経系は極めて精巧な神経回路網を有する。ごく最近、神経回路網の形成を担う様々な細胞外神経軸索ガイダンス因子が同定されてきた。しかし、それらの下流でどのような細胞内シグナル伝達分子が成長円錐の運動とそれに伴う軸索のガイダンスの制御を行うのかはほとんど理解されていない。私はRhoキナーゼの新規脳内標的蛋白質CRMP-2を同定した。そして、Rhoキナーゼ特異的なCRMP-2のリン酸化や成長円錐の形態変化をモニターすることによって、細胞外シグナル依存的な成長円錐の退縮にRhoキナーゼが重要な役割を果たすことを証明した。本研究では神経回路形成におけるRhoキナーゼとCRMP-2の機能とその作用メカニズムを解明することを目的する。本年度の研究業績は以下の通りである。 1)成長円錐の退縮を引き起こす事で知られるephrin-A5刺激によりDRG neuronにおいてCRMP-2のリン酸化が上昇することが確認され、その成長円錐の退縮をRhoキナーゼによりリン酸化されるアミノ酸をアスパラギン酸に変換したCRMP-2変異体(リン酸化されたCRMP-2を模倣したもの)が抑制しうることが明らかとなった。 2)電子顕微鏡をもちいた解析の結果、CRMP-2はDRG neuronの成長円錐において、microtubulesの上やClathrin-coated pitの上に存在していることが明らかとなった。 3)CRMP-2のRhoキナーゼによるリン酸化サイトを特異的に認識する抗体で解析した結果、リン酸化型CRMP-2はmicrotubulesの上やclathrin-coated pitの上に存在していないことが明らかとなった。 以上の結果からRhoキナーゼによるCRMP-2のリン酸化は、microtubulesやClathrin-coated pitへの相互作用を介して細胞骨格系に関与している可能性が示唆された。 以上のことから、平成15年度の研究計画はほぼ達成されたものと考える。

  17. Neuroscience Competitive

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Teaching Experience 3

  1. 薬効学特論　東北大学薬学部

  2. 機能形態学２　東北大学薬学部

  3. 薬理学１　東北大学薬学部