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Nariko Arimura, PhD

Associate Professor
Department of  Pharmacology
Graduate School of Pharmaceutical Sciences
Tohoku University

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Symposium organizer at JBS meeting 2022

The symposium titled "Down syndrome complex pathology produces neo-biochemistry from the basic to the clinic" took place during the 95th Annual Meeting of the Japanese Biochemical Society.



Our review titled  "Neuronal and astrocytic protein connections and associated adhesion molecules" was published  in Neuroscience Research.

Image by Markus Winkler

Prepaper submission to In Review

Our preprint was submitted to In Review, Journal-integrated preprint system sharing from Springer Nature and Research Square

Lecture Presentation

Symposium organizer at MBSJ 2021

“Brain functions enhanced by intercellular communication: new-found reciprocity of astrocytes and neurons” Symposium took place during the 44th Annual Meeting of the Molecular Biology Society of Japan. We greatly appreciate all the staff of the the Molecular Biology Society of Japan who worked diligently to set up the zoom conference under the continuing global pandemic. I’d like to express my gratitude to our invited speakers/dear friends: Dr. Jun Nagai (RIKEN), Dr. Nicola J Allen (Salk Institute) Dr. Tetsuya Takano (Keio University) and Dr. Schuichi Koizumi (University of Yamanashi). It was very successful and informative experience.


Our Research Topics was started in "Frontiers in Neuroscience"

I'm pleased to be launching a new Research Topic, Current Advances in the Study of Down Syndrome: from Development to Aging, together with Dr. Yann Herault, and Dr. William Mobley in Frontiers in Neuroscience


Paper acception by Science Advances

The scientific paper “ DSCAM Regulates Delamination of Neurons in the Developing Midbrain” was published in Science Advances. This manuscript highlights the involvement of DSCAM in the earliest molecular machinery of neuronal departure from the ventricular surface. Many thanks to all contributing authors for their intense cooperation.


Oral talk at The 64th Annual Meeting of the Japanease Society for Neurochemistry

"Synaptic reorganization by astrocytes and brain function” Symposium (S9) took place during the The 64th Annual Meeting of the Japanease Society for Neurochemistry online and I presented our recent studies.

I would like to thank the organizer, Dr. Koizumi, for inviting me to such a great symposium.


Oral talk at Neuroscience 2021

"Neurological diseases and cancer resulting from developmental deficiency in the cerebellum” Symposium (2S06a) took place during the Neuroscience 2021 online and I presented our recent studies.

I would like to thank the organizers, Dr. Kawauchi and Dr. Uesaka, for inviting me to such a wonderful symposium.

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Midbrain Development

The midbrain is a very important area involved in cognitive, emotional, and motor function control by secreting important neurotransmitters such as dopamine. In addition, the midbrain is considered to be the most developed in the very early stages of vertebrate brain evolution, preserving the molecular and morphological foundations that can form dense neural circuits. However, there are many unclear points about the developmental mechanisms of nerve cells in the midbrain.
Since many central nerve cells are located at different locations from where they are produced and where they actually function, they migrate after differentiating on the ventricular surface. Excitatory and inhibitory neurons in the cerebrum differentiate in completely different places and migrate to the cerebral cortex. On the other hand, in the mesencephalic nerve cells, various types of excitatory and inhibitory cells are produced ‘at the same time and in the same region’ from the limited ventricular surface and move to the same place, and this differentiation / migration control mechanism is mostly unknown. The phenomenon of excitatory and inhibitory cells differentiating and migrating in the same place is a phenomenon common to other regions composed of nerve nuclei such as pons and medulla oblongata, but the details have not been clarified. In addition, when neurons on the dorsal side of the midbrain (superior colliculus) are labeled in the short term, cells differentiated in the same region at the same time move and stop in each layer to form a rough layered structure. It is considered that there is an unexplained layer structure formation mechanism different from in the cerebrum and cerebellum. Thus, using the midbrain as a model system, now we trying to elucidate ‘how various differentiated nerve cells move to individual functioning places and stop.’


Molecular Function of DSCAM

DSCAM is a unique transmembrane protein that is responsible for “self-avoidance” in flies and mice (Hattori et al., Ann Rev Cell Dev, 2008). This cellular event is composed of two successive processes: recognition of allogenic cells and cancellation/masking of cell adhesion. Although it is known that the “recognition” process is elicited by the homophilic association of similar DSCAM variants, the molecular mechanism behind cancellation of cell adhesion remains unclear (Garrett et al., Proc Natl Acad Sci U S A, 2018).
In our recent study, we clarified that DSCAM accumulates at the detachment sites of endfeet and mediates neuronal delamination via the RapGEF2-Rap1-N-cadherin signaling cascade. (Arimura et al., Science Advances, 2020). Our manuscript highlights at least three major novel findings: 1) the involvement of DSCAM in the earliest molecular machinery of neuronal departure from the ventricular surface, 2) the suppression of N-cadherin by DSCAM-Rap1/RapGEF2 signaling cascade in neuronal detachment, and 3) the molecular mechanisms by which DSCAM cancels the activities of other cell adhesion molecules. This study provides important clues to understanding the molecular mechanisms by which newborn neurons detach from the ventricular surface upon their neuronal fate commitment. Our findings shed light on the key cellular machinery regulating proper cell tiling and avoiding allogenic neurite fasciculation, which is fundamental in normal neurogenesis and circuit formation.

Home: プロジェクト


1. Dewa K, Arimura N. Neuronal and astrocytic protein connections and associated adhesion molecules. doi: 10.1016/j.neures.2022.09.014. Online ahead of print. 2022.

2. Yamashiro K, Hori K, Lai ESK, Aoki R, Shimaoka K, Arimura N, Egusa SF, Sakamoto A, Abe M, Sakimura K, Watanabe T, Uesaka N, Kano M, Hoshino M. AUTS2 Governs Cerebellar Development, Purkinje Cell Maturation, Motor Function and Social Communication.

iScience. 23(12):101820, 2020.

3. Arimura. N*, Okada M, Taya S, Dewa K, Tsuzuki A, Uetake H, Miyashita S, Hashizume K, Shimaoka K, Egusa S, Nishioka T, Yanagawa Y, Yamakawa K, Inoue Y, Inoue T, Kaibuchi K, Hoshino M. DSCAM regulates delamination of neurons in the developing midbrain.

Science Advances, 2020 6(36), eaba1693. (*: co-corresponding author)

4. Arimura N*, Dewa K, Okada M, Yanagawa Y, Taya S, Hoshino M. Comprehensive and cell type-based characterization of the dorsal midbrain during development.

Genes to Cells, 179(4), 1273-1284, 2019. (*: co-corresponding author)

5. Watanabe T, Kakeno M, Matsui T, Sugiyama I, Arimura N, Matsuzawa K, Shirahige A, Ishidate F, Nishioka T, Taya S, Hoshino M, Kaibuchi K. TTBK with EB1/3 regulates microtubule dynamics in migrating cells through KIF2A phosphorylation.

Journal of Cell Biology, 210(5), 737-751, 2015.

6. Arimura N, Nakayama Y, Yamagata T, Tanji J, Hoshi E. Involvement of the globus pallidus in behavioral goal determination and action specification.

Journal of Neuroscience, 33, 13639-53, 2013

7. Nakamuta S, Funahashi Y, Namba T, Arimura N, Picciotto MR, Tokumitsu H, Soderling TR, Sakakibara A, Miyata T, Kamiguchi H, and Kaibuchi K. Local application of Neurotrophins specifies axon through inositol 1, 4, 5-trisphosphate/Ca2+/calmodulin-dependent protein kinases.

Science Signalling, 4(199):ra76, 2011

8. Arimura N, Kimura T, Nakamuta, S, Taya S, Funahashi Y, Hattori A, Shimada A, Ménager C, Kawabata S, Fujii K, Iwamatsu A, Segal RA, Fukuda M, & Kaibuchi K. Direct interaction of Slp1 and Rab27 with TrkB receptor regulates its anterograde transport in axons.

Developmental Cell 16. 1-12, 2009.

9. Arimura N, Hattori A, Kimura T, Nakamuta S, Funahashi Y, Hirotsune S, Furuta K, Urano T, Toyoshima YY, Kaibuchi K. CRMP-2 directly binds to cytoplasmic dynein and interferes with its activity.

Journal of Neurochemistry 111(2), 380-90, 2009.

10. Iguchi Y, Katsuno M, Niwa J, Yamada S, Sone J, Waza M, Adachi H, Tanaka F, Nagata K, Arimura N, Watanabe T, Kaibuchi K, Sobue G. TDP-43 depletion induces neuronal cell damage through dysregulation of Rho family GTPases.

Journal of Biological Chemistry 284, 22059-66, 2009.

11. Patrakitkomjorn S, Kobayashi D, Morikawa T, Wilson MM, Tsubota N, Irie A, Ozawa T, Aoki M, Arimura N, Kaibuchi K, Saya H, & Araki N. Neurofibromatosis type 1 (NF1) tumor suppressor, neurofibromin, regulates the neuronal differentiation of PC12 cells via its associating protein, CRMP-2.

Journal of Biological Chemistry 283, 9399-413, 2008.

12. Arimura N & Kaibuchi K. Neuronal polarity: from extracellular signals to intracellular mechanisms.

Nature Review Neuroscience 8, 194-205, 2007.

13. Wang S, Watanabe T, Noritake J, Fukata M, Yoshimura T, Itoh N, Harada T, Nakagawa M, Matsuura Y, Arimura N & Kaibuchi K. IQGAP3, a novel effector of Rac1 and Cdc42, regulates neurite outgrowth.

Journal of Cellular Science 120, 567-77, 2007.

14. Mimura F, Yamagishi S, Arimura N, Fujitani M, Kubo T, Kaibuchi K & Yamashita T. MAG inhibits microtubule assembly by a Rho-kinase dependent mechanism.

Journal of Biological Chemistry 281, 15970-9, 2006.

15. Yoshimura T, Arimura N, & Kaibuchi K. Signaling networks in neuronal polarization.

Journal of Neuroscience 26, 10626-30, 2006.

16. Oguri T, Inoko A, Shima H, Izawa I, Arimura N, Yamaguchi T, Inagaki N, Kaibuchi K, Kikuchi K & Inagaki M. Vimentin-Ser82 as a memory phosphorylation site in astrocytes.

Genes to Cells 11(5), 531-40, 2006.

17. Yoshimura T, Kawano Y, Arimura N, Kawabata S, Kikuchi A, & Kaibuchi K. GSK-3β regulates phosphorylation of CRMP-2 and neuronal polarity.

Cell 120, 137-49, 2005.

18. Arimura N, Menager C, Kawano Y, Yoshimura T, Kawabata S, Hattori A, Fukata Y, AmanoM, Goshima Y, Inagaki M, Morone M, Usukura J, & Kaibuchi K. Phosphorylation by Rho-kinase regulates CRMP-2 activity in growth cones.

Molecular and Cellular Biology 25, 9973-84, 2005.

19. Kimura T*, Arimura N*, Fukata Y, Watanabe H, Iwamatsu A, & Kaibuchi K. Tubulin and CRMP-2 complex is transported via Kinesin-1.

Journal of Neurochemistry 93(6), 1371-82, 2005. (*: equal contribution)

20. Jaillard C, Harrison S, Stankoff B, Aigrot MS, Calver AR, Duddy G, Walsh FS, Pangalos MN, Arimura N, Kaibuchi K, Zalc B & Lubetzki C. Edg8/S1P5: an oligodendroglial receptor with dual function on process retraction and cell survival.

Journal of Neuroscience 25(6), 1459-69. 2005.

21. Arimura N, & Kaibuchi K. Key Regulators in Neuronal Polarity.

Neuron 48, 881-4, 2005.

22. Meager C, Arimura N, Fukata Y, & Kaibuchi K. PIP3 is involved in neuronal polarization and axon formation.

Journal of Neurochemistry 89(1), 109-18, 2004.

23. Arimura N, Menager C, Fukata Y, & Kaibuchi K. Role of CRMP-2 in neuronal polarity.

Journal of Neurobiology 58(1), 34-47, 2004.

24. Inagaki N, Chihara K, Arimura N, Menager C, Kawano Y, Matsuo N, Nishimura T, Amano M, & Kaibuchi K. CRMP-2 induces axons in cultured hippocampal neurons.

Nature Neuroscience 4(8), 781-2, 2001.

25. Arimura N, Inagaki N, Chihara K, Menager C, Nakamura N, Amano M, Iwamatsu A, Goshima Y, & Kaibuchi K. Phosphorylation of collapsin response mediator protein-2 by Rho-kinase. Evidence for two separate signaling pathways for growth cone collapse.

Journal of Biological Chemistry 275(31), 23973-80, 2000.

25. Inagaki N, Nishizawa M, Arimura N, Yamamoto H, Takeuchi Y, Miyamoto E, Kaibuchi K, & Inagaki M. Activation of Ca2+/calmodulin-dependent protein kinase II within post-synaptic dendritic spines of cultured hippocampal neurons.

Journal of Biological Chemistry 275(35), 27165-71, 2000.

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Japanese Books

1. 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:認知と運動の統合過程を支える神経基盤、Brain and Nerve、63(1): 59-68, 2011

2. 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:補足運動野と前補足運動野、Clinical Neuroscience、28(10): 1121-24, 2010

3. 有村奈利子、吉村武、貝淵弘三:神経細胞の極性制御機構、蛋白質核酸酵素、53, 4, 386-392, 2008

4. 吉村武、有村奈利子、服部敦志、貝淵弘三: 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、蛋白質核酸酵素、52, 7, 753-756, 2007

5. 吉村武、有村奈利子、貝淵弘三、神経細胞の極性形成に関与する分子の網羅的解析、細胞工学、25, 6, 636-641、2006

6. 有村奈利子、吉村武、貝淵弘三:神経極性、蛋白質核酸酵素、51, 6, 786-795, 2006

7. 有村奈利子、吉村武、川端紗枝子、服部敦志、貝淵弘三:リン酸化が制御する神経細胞極性化の新規メカニズム、実験医学23, 13, 2012-2016, 2005

8. 吉村武、河野洋治、有村奈利子、川端紗枝子、貝淵弘三:神経細胞の極性を司る分子機構、日本神経精神薬理学雑誌、25、4, 169-174、2005

9. 吉村武、河野洋治、有村奈利子、川端紗枝子、貝淵弘三:神経細胞の極性を制御する分子機構、細胞工学、24、3、231-235、2005

10. 有村奈利子、木村俊秀、藤井佳代、貝淵弘三、神経軸索伸長における細胞骨格制御機構、細胞工学、23、9、1047-1051、2005

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I am a neuroscientist, wife, and mother of two wonderful daughters. Currently, I reside in Sendai. In my free time, I enjoy reading ‘bunkoban’ novels, watching movies, and window shopping. When I was a high school student, I wanted to be a foreign diplomat because I wanted to travel abroad, but thought it would be too difficult, so I decided to be a neuroscientist instead. I love travelling (for scientific meeting) and have been to San Diego and Washington in the USA, Lion in France, Beijing in China, and Lisbon in Portugal. Someday I hope to visit Brazil and Singapore.

We are researching DSCAM functions in the midbrain. Please see the details of our research page. Our team has published several papers on our research and we recently presented at a symposium online. We are planning to present at four more symposiums in 2021 at this time.  We are looking for overseas partners to cooperate with us on…

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Department of  Pharmacology

Graduate School of Pharmaceutical Sciences

Tohoku University

6-3 Aoba, Aramaki, Aoba-ku, Sendai 980-8578, Japan


〒980-8578 宮城県仙台市青葉区荒巻字青葉6-3

東北大学大学院薬学研究科A棟 3階




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