Updated on 2025/07/04

写真a

 
SATO Tokiharu
 
Organization
Brain Research Institute Assistant Professor
Title
Assistant Professor
External link

Degree

  • 博士(医学) ( 2008.12   金沢大学 )

Research Interests

  • 神経変性

  • 神経再生

  • 神経科学

Research Areas

  • Life Science / Anatomy and histopathology of nervous system

Research History (researchmap)

  • Niigata University   Brain Research Institute   Assistant Professor

    2021.12

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  • Niigata University   Brain Research Institute   Specially Appointed Assistant Professor

    2019.2 - 2021.11

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  • Department of Neurobiology and Anatomy, McGovern Medical School at the University of Texas Medical School at Houston

    2015.10 - 2019.1

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  • Kanazawa University   Cancer Research Institute   Assistant Professor

    2012.4 - 2015.9

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  • Kanazawa University   Assistant Professor

    2009.1 - 2012.3

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Research History

  • Niigata University   Brain Research Institute   Assistant Professor

    2021.12

  • Niigata University   Brain Research Institute Center for Bioresources   Specially Appointed Assistant Professor

    2019.2

Education

  • Kanazawa University   医学系研究科

    - 2008.12

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    Country: Japan

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  • Kanazawa University   Graduate School, Division of Medical Sciences

    - 2008

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Professional Memberships

 

Papers

  • TDP-43 mutants with different aggregation properties exhibit distinct toxicity, axonal transport, and secretion for disease progression in a mouse ALS/FTLD model Reviewed

    Hideki Mori, Tokiharu Sato, Shintaro Tsuboguchi, Masahiko Takahashi, Yuka Nakamura, Kana Hoshina, Taisuke Kato, Masahiro Fujii, Osamu Onodera, Masaki Ueno

    Neurobiology of Disease   212   106988 - 106988   2025.8

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    Authorship:Lead author   Publishing type:Research paper (scientific journal)   Publisher:Elsevier BV  

    DOI: 10.1016/j.nbd.2025.106988

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  • Scg2 drives reorganization of the corticospinal circuit with spinal premotor interneurons to recover motor function after stroke

    Tokiharu Sato, Yuka Nakamura, Kana Hoshina, Ken-ichi Inoue, Masahiko Takada, Masato Yano, Hitoshi Matsuzawa, Masaki Ueno

    bioRxiv   2025.1

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    <jats:title>Abstract</jats:title><jats:p>Brain injuries such as stroke damage neural circuitry and lead to functional deficits. Spared motor pathways are often reorganized and contribute to functional recovery; however, the connectivity and molecular mechanisms that drive the reorganization are largely unknown. Here, we demonstrate structural and functional connectivity reformed by spared corticospinal axons after stroke and determine a key secretory protein that drives the reorganization. We first found that corticospinal axons innervate specific areas of the denervated cervical cord after stroke. Anatomical and photometric analyses reveal that the axons reconnect to premotor V2a interneurons. Kinematic analyses of forelimb movements and chemogenetic silencing reveal their contribution to motor recovery. Translated mRNA expression analyses of V2a interneurons and astrocytes in the denervated cervical cord reveal diverse transcripts upregulated in the rewiring process. In particular, a secretory protein Scg2 is upregulated by injury-induced purinergic ATP signals and rehabilitative training-induced neural activity and possesses an ability to promote axon growth via cAMP and S6 signaling. Scg2 overexpression in the denervated cervical cord enhances axon rewiring, while the Scg2 knockdown attenuates it. The present data reveal the neural substrate and molecular mechanism essential to induce reorganization and recovery of the motor system, providing fundamental therapeutic targets for CNS injuries.</jats:p>

    DOI: 10.1101/2025.01.21.634186

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  • CRISPR/CasRx suppresses KRAS-induced brain arteriovenous malformation developed in postnatal brain endothelial cells in mice Reviewed

    Shoji Saito, Yuka Nakamura, Satoshi Miyashita, Tokiharu Sato, Kana Hoshina, Masayasu Okada, Hitoshi Hasegawa, Makoto Oishi, Yukihiko Fujii, Jakob Körbelin, Yoshiaki Kubota, Kazuki Tainaka, Manabu Natsumeda, Masaki Ueno

    JCI Insight   9 ( 22 )   2024.11

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:American Society for Clinical Investigation  

    DOI: 10.1172/jci.insight.179729

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  • TDP-43は運動回路の変性を誘導するために異なって伝播する(TDP-43 differentially propagates to induce degeneration in the motor circuit)

    坪口 晋太朗, 中村 由香, 石原 智彦, 加藤 泰介, 佐藤 時春, 小山 哲秀, 森 秀樹, 小池 佑佳, 小野寺 理, 上野 将紀

    Dementia Japan   37 ( 4 )   680 - 680   2023.10

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    Language:English   Publisher:(一社)日本認知症学会  

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  • TDP-43 differentially propagates to induce antero- and retrograde degeneration in the corticospinal circuits in mouse focal ALS models. Reviewed International journal

    Shintaro Tsuboguchi, Yuka Nakamura, Tomohiko Ishihara, Taisuke Kato, Tokiharu Sato, Akihide Koyama, Hideki Mori, Yuka Koike, Osamu Onodera, Masaki Ueno

    Acta neuropathologica   2023.8

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    Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease characterized by TDP-43 inclusions in the cortical and spinal motor neurons. It remains unknown whether and how pathogenic TDP-43 spreads across neural connections to progress degenerative processes in the cortico-spinal motor circuitry. Here we established novel mouse ALS models that initially induced mutant TDP-43 inclusions in specific neuronal or cell types in the motor circuits, and investigated whether TDP-43 and relevant pathological processes spread across neuronal or cellular connections. We first developed ALS models that primarily induced TDP-43 inclusions in the corticospinal neurons, spinal motor neurons, or forelimb skeletal muscle, by using adeno-associated virus (AAV) expressing mutant TDP-43. We found that TDP-43 induced in the corticospinal neurons was transported along the axons anterogradely and transferred to the oligodendrocytes along the corticospinal tract (CST), coinciding with mild axon degeneration. In contrast, TDP-43 introduced in the spinal motor neurons did not spread retrogradely to the cortical or spinal neurons; however, it induced an extreme loss of spinal motor neurons and subsequent degeneration of neighboring spinal neurons, suggesting a degenerative propagation in a retrograde manner in the spinal cord. The intraspinal degeneration further led to severe muscle atrophy. Finally, TDP-43 induced in the skeletal muscle did not propagate pathological events to spinal neurons retrogradely. Our data revealed that mutant TDP-43 spread across neuro-glial connections anterogradely in the corticospinal pathway, whereas it exhibited different retrograde degenerative properties in the spinal circuits. This suggests that pathogenic TDP-43 may induce distinct antero- and retrograde mechanisms of degeneration in the motor system in ALS.

    DOI: 10.1007/s00401-023-02615-8

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  • Cerebrospinal fluid-contacting neuron tracing reveals structural and functional connectivity for locomotion in the mouse spinal cord. Reviewed International journal

    Yuka Nakamura, Miyuki Kurabe, Mami Matsumoto, Tokiharu Sato, Satoshi Miytashita, Kana Hoshina, Yoshinori Kamiya, Kazuki Tainaka, Hitoshi Matsuzawa, Nobuhiko Ohno, Masaki Ueno

    eLife   12   e83108   2023.2

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    Cerebrospinal fluid-contacting neurons (CSF-cNs) are enigmatic mechano- or chemosensory cells lying along the central canal of the spinal cord. Recent studies in zebrafish larvae and lampreys have shown that CSF-cNs control postures and movements via spinal connections. However, the structures, connectivity, and functions in mammals remain largely unknown. Here we developed a method to genetically target mouse CSF-cNs that highlighted structural connections and functions. We first found that intracerebroventricular injection of adeno-associated virus with a neuron-specific promoter and Pkd2l1-Cre mice specifically labeled CSF-cNs. Single-cell labeling of 71 CSF-cNs revealed rostral axon extensions of over 1800 μm in unmyelinated bundles in the ventral funiculus and terminated on CSF-cNs to form a recurrent circuitry, which was further determined by serial electron microscopy and electrophysiology. CSF-cNs were also found to connect with axial motor neurons and premotor interneurons around the central canal and within the axon bundles. Chemogenetic CSF-cNs inactivation reduced speed and step frequency during treadmill locomotion. Our data revealed the basic structures and connections of mouse CSF-cNs to control spinal motor circuits for proper locomotion. The versatile methods developed in this study will contribute to further understanding of CSF-cN functions in mammals.

    DOI: 10.7554/eLife.83108

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  • Lesion Area in the Cerebral Cortex Determines the Patterns of Axon Rewiring of Motor and Sensory Corticospinal Tracts After Stroke Reviewed

    Tokiharu Sato, Yuka Nakamura, Akinori Takeda, Masaki Ueno

    Frontiers in Neuroscience   15   2021.10

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:Frontiers Media SA  

    The corticospinal tract (CST) is an essential neural pathway for reorganization that recovers motor functions after brain injuries such as stroke. CST comprises multiple pathways derived from different sensorimotor areas of the cerebral cortex; however, the patterns of reorganization in such complex pathways postinjury are largely unknown. Here we comprehensively examined the rewiring patterns of the CST pathways of multiple cerebral origins in a mouse stroke model that varied in size and location in the sensorimotor cortex. We found that spared contralesional motor and sensory CST axons crossed the midline and sprouted into the denervated side of the cervical spinal cord after stroke in a large cortical area. In contrast, the contralesional CST fibers did not sprout in a small stroke, whereas the ipsilesional axons from the spared motor area grew on the denervated side. We further showed that motor and sensory CST axons did not innervate the projecting areas mutually when either one was injured. The present results reveal the basic principles that generate the patterns of CST rewiring, which depend on stroke location and CST subtype. Our data indicate the importance of targeting different neural substrates to restore function among the types of injury.

    DOI: 10.3389/fnins.2021.737034

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  • Direct Comparison of Odor Responses of Homologous Glomeruli in the Medial and Lateral Maps of the Mouse Olfactory Bulb Reviewed

    Tokiharu Sato, Ryota Homma, Shin Nagayama

    eneuro   7 ( 2 )   ENEURO.0449 - 19.2020   2020.1

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:Society for Neuroscience  

    Abstract

    Olfactory sensory neurons (OSNs) expressing same-type odorant receptors typically project to a pair of glomeruli in the medial and lateral sides of the olfactory bulbs (OBs) in rodents. This multiple glomerular representation of homologous inputs is considered to have more important functional roles for odor information processing than the redundant backup system. However, a consensus idea is lacking and this hinders interpretation of the phenomenon. In addition, the shared and unique odorant response properties of the homologous glomeruli remain unclear because the majority of medial glomeruli are hidden in the septal OB, and thus it is difficult to directly compare them. OSNs, which express trace amine-associated odorant receptors (TAARs), were recently identified that project to a pair of glomeruli uniquely located in the dorsal OB. In this study, we measured the odorant-induced calcium responses of homologous pairs of TAAR glomeruli simultaneously in anesthetized mice and directly compared their response patterns. We found that they exhibited similar temporal response patterns and could not find differences in onset latency, rise time, decay time, or response amplitude. However, the medial glomeruli had significantly larger respiration-locked calcium fluctuations than the lateral glomeruli. This trend was observed with/without odorant stimulation in postsynaptic neurons of GABAergic, dopaminergic, and mitral/tufted cells, but not in presynaptic olfactory sensory axon terminals. This indicates that, at least in these TAAR glomeruli, the medial rather than the lateral OB map enhances the respiration-locked rhythm and transfers this information to higher brain centers.

    DOI: 10.1523/eneuro.0449-19.2020

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  • Narrowly Confined and Glomerulus-Specific Onset Latencies of Odor-Evoked Calcium Transients in the Juxtaglomerular Cells of the Mouse Main Olfactory Bulb Reviewed

    Ryota Homma, Xiaohua Lv, Tokiharu Sato, Fumiaki Imamura, Shaoqun Zeng, Shin Nagayama

    eneuro   6 ( 1 )   ENEURO.0387 - 18.2019   2019.1

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:Society for Neuroscience  

    Abstract

    Odor information is transmitted from olfactory sensory neurons to principal neurons at the glomeruli of the olfactory bulb. The intraglomerular neuronal circuit also includes hundreds of interneurons referred to as juxtaglomerular (JG) cells. Stimulus selectivity is well correlated among many JG cells that are associated with the same glomerulus, consistent with their highly homogeneous sensory inputs. However, much less is known about the temporal aspects of their activity, including the temporal coordination of their odor-evoked responses. As many JG cells within a glomerular module respond to the same stimulus, the extent to which their activity is temporally aligned will affect the temporal profile of their population inhibitory inputs. Using random-access high-speed two-photon microscopy, we recorded the odor-evoked calcium transients of mouse JG cells and compared the onset latency and rise time among neurons putatively associated with the same and different glomeruli. Whereas the overall onset latencies of odor-evoked transients were distributed across a ∼150 ms time window, those from cells putatively associated with the same glomerulus were confined to a much narrower window of several tens of milliseconds. This result suggests that onset latency primarily depends on the associated glomerulus. We also observed glomerular specificity in the rise time. The glomerulus-specific temporal pattern of odor-evoked activity implies that the temporal patterns of inputs from the intraglomerular circuit are unique to individual glomerulus–odor pairs, which may contribute to efficient shaping of the temporal pattern of activity in the principal neurons.

    DOI: 10.1523/eneuro.0387-18.2019

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  • The osteopontin-CD44 axis in hepatic cancer stem cells regulates IFN signaling and HCV replication. Reviewed International journal

    Takayoshi Shirasaki, Masao Honda, Taro Yamashita, Kouki Nio, Tetsuro Shimakami, Ryougo Shimizu, Saki Nakasyo, Kazuhisa Murai, Natsumi Shirasaki, Hikari Okada, Yoshio Sakai, Tokiharu Sato, Tetsuro Suzuki, Katsuji Yoshioka, Shuichi Kaneko

    Scientific reports   8 ( 1 )   13143 - 13143   2018.9

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    Osteopontin (OPN) is involved in cell proliferation, migration, inflammation, and tumor progression in various tissues. OPN induces stemness by interacting with CD44, but the functional relevance of OPN-mediated interferon (IFN) signaling and hepatitis C virus (HCV) replication in stem cell populations remains unclear. In this study, we investigated the effect of OPN on HCV replication and IFN signaling in cancer stem cells (CSCs) positive for epithelial cell adhesion molecule (EpCAM) and CD44. We show that the EpCAM+/CD44+ CSCs show marked HCV replication when compared to EpCAM-/CD44- cells. In addition, OPN significantly enhances this HCV replication in EpCAM+/CD44+ CSCs and markedly suppresses IFN-stimulated gene expression. The GSK-3β inhibitor BIO increases the EpCAM+/CD44+ CSC population and OPN expression and impairs IFN signaling via STAT1 degradation. Taken together, our data suggest that OPN enhances HCV replication in the EpCAM+/CD44+ CSCs, while it also negatively regulates the IFN signaling pathway via inhibition of STAT1 phosphorylation and degradation. Therefore, OPN may represent a novel therapeutic target for treating HCV-related hepatocellular carcinoma.

    DOI: 10.1038/s41598-018-31421-6

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  • Critical role of JSAP1 and JLP in axonal transport in the cerebellar Purkinje cells of mice Reviewed

    Tokiharu Sato, Momoe Ishikawa, Toru Yoshihara, Ryota Nakazato, Haruhiro Higashida, Masahide Asano, Katsuji Yoshioka

    FEBS LETTERS   589 ( 19 )   2805 - 2811   2015.9

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    DOI: 10.1016/j.febslet.2015.08.024

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  • JSAP1/JIP3 and JLP regulate kinesin-1-dependent axonal transport to prevent neuronal degeneration Reviewed

    T. Sato, M. Ishikawa, M. Mochizuki, M. Ohta, M. Ohkura, J. Nakai, N. Takamatsu, K. Yoshioka

    CELL DEATH AND DIFFERENTIATION   22 ( 8 )   1260 - 1274   2015.8

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    DOI: 10.1038/cdd.2014.207

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  • JSAP1 and JLP are required for ARF6 localization to the midbody in cytokinesis Reviewed

    Baljinnyam Tuvshintugs, Tokiharu Sato, Radnaa Enkhtuya, Katsumi Yamashita, Katsuji Yoshioka

    GENES TO CELLS   19 ( 9 )   692 - 703   2014.9

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    DOI: 10.1111/gtc.12170

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  • The scaffold protein JLP plays a key role in regulating ultraviolet B-induced apoptosis in mice Reviewed

    Radnaa Enkhtuya, Tokiharu Sato, Mitsuo Wakasugi, Baljinnyam Tuvshintugs, Hirofumi Miyata, Takeshi Sakurai, Tsukasa Matsunaga, Katsuji Yoshioka

    GENES TO CELLS   19 ( 4 )   350 - 358   2014.4

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    DOI: 10.1111/gtc.12135

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  • Human microRNA-1245 down-regulates the NKG2D receptor in natural killer cells and impairs NKG2D-mediated functions Reviewed

    J. Luis Espinoza, Akiyoshi Takami, Katsuji Yoshioka, Katsuya Nakata, Tokiharu Sato, Yoshihito Kasahara, Shinji Nakao

    HAEMATOLOGICA-THE HEMATOLOGY JOURNAL   97 ( 9 )   1295 - 1303   2012.9

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    DOI: 10.3324/haematol.2011.058529

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  • Role of plasma membrane localization of the scaffold protein JSAP1 during differentiation of cerebellar granule cell precursors Reviewed

    Tokiharu Sato, Anir Enkhbat, Katsuji Yoshioka

    GENES TO CELLS   16 ( 1 )   58 - 68   2011.1

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    DOI: 10.1111/j.1365-2443.2010.01465.x

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  • Ablation of the scaffold protein JLP causes reduced fertility in male mice. Reviewed International journal

    Iwanaga A, Wang G, Gantulga D, Sato T, Baljinnyam T, Shimizu K, Takumi K, Hayasi M, Akashi T, Fuse H, Sugihara K, Asano M, Yoshioka K

    Transgenic Research   17 ( 6 )   1045 - 1058   2008.12

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    The specific and efficient activation of mitogen-activated protein kinase (MAPK) signaling modules is mediated, at least in part, by scaffold proteins. c-Jun NH(2)-terminal kinase (JNK)-associated leucine zipper protein (JLP) was identified as a scaffold protein for JNK and p38 MAPK signaling modules. JLP is expressed nearly ubiquitously and is involved in intracellular signaling pathways, such as the G(alpha13) and Cdo-mediated pathway, in vitro. To date, however, JLP expression has not been analyzed in detail, nor are its physiological functions well understood. Here we investigated the expression of JLP in the mouse testis during development. Of the tissues examined, JLP was strongest in the testis, with the most intense staining in the elongated spermatids. Since the anti-JLP antibody used in this study can recognize both JLP and sperm-associated antigen 9 (SPAG9), a splice variant of JLP that has been studied extensively in primates, we also examined its expression in macaque testis samples. Our results indicated that in mouse and primate testis, the isoform expressed at the highest level was JLP, not SPAG9. We also investigated the function of JLP by disrupting the Jlp gene in mice, and found that the male homozygotes were subfertile. Taken together, these observations may suggest that JLP plays an important role in testis during development, especially in the production of functionally normal spermatozoa.

    DOI: 10.1007/s11248-008-9191-6

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  • Ablation of the scaffold protein JLP causes reduced fertility in male mice Reviewed

    Asuka Iwanaga, Guangmin Wang, Davaakhuu Gantulga, Tokiharu Sato, Tuvshintugs Baljinnyam, Keiko Shimizu, Ken Takumi, Motoharu Hayashi, Takuya Akashi, Hideki Fuse, Kazushi Sugihara, Masahide Asano, Katsuji Yoshioka

    Transgenic Research   17 ( 6 )   1045 - 1058   2008.12

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    DOI: 10.1007/s11248-008-9191-6

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  • The scaffold protein JSAP1 regulates proliferation and differentiation of cerebellar granule cell precursors by modulating JNK signaling Reviewed

    Tokiharu Sato, Takashi Torashima, Kazushi Sugihara, Hirokazu Hirai, Masahide Asano, Katsuji Yoshioka

    MOLECULAR AND CELLULAR NEUROSCIENCE   39 ( 4 )   569 - 578   2008.11

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    Authorship:Lead author   Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1016/j.mcn.2008.08.003

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  • Neural-specific ablation of the scaffold protein JSAP1 in mice causes neonatal death Reviewed

    Asuka Iwanaga, Tokiharu Sato, Kazushi Sugihara, Atsushi Hirao, Nobuyuki Takakura, Hiroshi Okamoto, Masahide Asano, Katsuji Yoshioka

    NEUROSCIENCE LETTERS   429 ( 1 )   43 - 48   2007.12

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    DOI: 10.1016/j.neulet.2007.09.057

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  • Expression and distribution of JNK/SAPK-associated scaffold protein JSAP1 in developing and adult mouse brain. Reviewed International journal

    Miura E, Fukaya M, Sato T, Sugihara K, Asano M, Yoshioka K, Watanabe M

    Journal of neurochemistry   97 ( 5 )   1431 - 1446   2006.6

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    The c-Jun N-terminal kinase (JNK) is one of the three major mitogen-activated protein kinases (MAPKs) playing key roles in various cellular processes in response to both extracellular and intracellular stimuli. JNK/SAPK-associated protein 1 (JSAP1 also referred to as JIP3) is a JNK-associated scaffold that controls the specificity and efficiency of JNK signaling cascades. Here we studied its expression in mouse brains. JSAP1 mRNA was expressed in developing and adult brains, showing spatial patterns similar to JNK1-3 mRNAs. In embryos, JSAP1 immunolabeling was intense for progenitor cells in the ventricular zone throughout the brain and in the external granular layer of the cerebellum, and for neurons and glial cells differentiating in the mantle zone. In adults, JSAP1 was distributed in various neurons and Bergmann glia, with higher levels in striatal cholinergic interneurons, telencephalic parvalbumin-positive interneurons and cerebellar Purkinje cells. In these neurons, JSAP1 was observed as tiny particulate staining in spines, dendrites, perikarya and axons, where it was often associated with the smooth endoplasmic reticulum (sER) and cell membrane. Immunoblots revealed enriched distribution in the microsomal fraction and cytosolic fraction. Therefore, the characteristic cellular expression and subcellular distribution of JSAP1 might be beneficial for cells to efficiently link external stimuli to the JNK MAPK pathway and other intracellular machineries.

    DOI: 10.1111/j.1471-4159.2006.03835.x

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  • Expression and distribution of JNK/SAPK-associated scaffold protein JSAP1 in developing and adult mouse brain Reviewed

    Eriko Miura, Masahiro Fukaya, Tokiharu Sato, Kazushi Sugihara, Masahide Asano, Katsuji Yoshioka, Masahiko Watanabe

    Journal of Neurochemistry   97 ( 5 )   1431 - 1446   2006.6

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    DOI: 10.1111/j.1471-4159.2006.03835.x

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  • Expression and distribution of JNK/SAPK-associated scaffold protein JSAP1 in mouse brain Reviewed

    Miura Eriko, Fukaya Masahiro, Sato Tokiharu, Sugihara Kazushi, Asano Masahide, Yoshioka Katsuji, Watanabe Masahiko

    NEUROSCIENCE RESEARCH   55   S179   2006

  • Impairment of cardiomyogenesis in embryonic stem cells lacking scaffold protein JSAP1 Reviewed

    T Sato, K Hidaka, A Iwanaga, M Ito, M Asano, Y Nakabeppu, T Morisaki, K Yoshioka

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS   338 ( 2 )   1152 - 1157   2005.12

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    DOI: 10.1016/j.bbrc.2005.10.052

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  • JSAP1/JIP3 cooperates with focal adhesion kinase to regulate c-Jun N-terminal kinase and cell migration Reviewed

    T Takino, M Nakada, H Miyamori, Y Watanabe, T Sato, D Gantulga, K Yoshioka, KM Yamada, H Sato

    JOURNAL OF BIOLOGICAL CHEMISTRY   280 ( 45 )   37772 - 37781   2005.11

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    DOI: 10.1074/jbc.M505241200

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  • Structure, regulation, and function of micro1 in the sea urchin Hemicentrotus pulcherrimus Reviewed

    Y Nishimura, T Sato, Y Morita, A Yamazaki, K Akasaka, M Yamaguchi

    DEVELOPMENT GENES AND EVOLUTION   214 ( 11 )   525 - 536   2004.11

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    DOI: 10.1007/s00427-004-0442-0

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MISC

  • 脳梗塞後における皮質脊髄路の再編様式と分子機序 Invited

    Medical Science Digest   50 ( 6 )   48 - 50   2024.5

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    Authorship:Lead author   Language:Japanese   Publishing type:Article, review, commentary, editorial, etc. (scientific journal)  

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  • TDP-43 differentially propagates to induce degeneration in the motor circuit

    坪口晋太朗, 中村由香, 石原智彦, 加藤泰介, 佐藤時春, 小山哲秀, 森秀樹, 小池佑佳, 小野寺理, 小野寺理, 上野将紀

    Dementia Japan   37 ( 4 )   2023

  • TDP-43変異型により異なる病態進展特性の解析

    森秀樹, 坪口晋太朗, 佐藤時春, 中村由香, 加藤泰介, 須貝章弘, 小野寺理, 上野将紀

    Dementia Japan   37 ( 4 )   2023

  • 脳・脊髄障害後の神経回路再編の可視化 Invited

    CLINICAL NEUROSCIENCE   40 ( 6 )   746 - 749   2022.6

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  • Intracortical and corticospinal spreading of TDP-43 in mouse FTLD/ALS models(和訳中)

    坪口 晋太朗, 中村 由香, 石原 智彦, 加藤 泰介, 小山 哲秀, 佐藤 時春, 吉田 富, 上野 将紀, 小野寺 理

    Dementia Japan   34 ( 4 )   524 - 524   2020.10

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  • FTLD/ALSモデルマウスにおけるTDP-43の皮質内と皮質脊髄内での増殖(Intracortical and corticospinal spreading of TDP-43 in mouse FTLD/ALS models)

    坪口 晋太朗, 中村 由香, 石原 智彦, 加藤 泰介, 小山 哲秀, 佐藤 時春, 吉田 富, 上野 将紀, 小野寺 理

    Dementia Japan   34 ( 4 )   524 - 524   2020.10

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  • Spreading of TDP-43 via direct corticospinal connections in mouse models

    TSUBOGUCHI Shintaro, NAKAMURA Yuka, ISHIHARA Tomohiko, KATO Taisuke, KOYAMA Akihide, SATO Tokiharu, YOSHIDA Yutaka, UENO Masaki, ONODERA Osamu

    日本神経学会学術大会プログラム・抄録集   61st   2020

  • 「匂い地図」として表現される匂い情報の処理基盤とその神経回路機構 Invited

    SATO Tokiharu

    AROMA RESEARCH   19 ( 4 )   2018

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  • A cell-autonomous role for JSAP1 and JLP in mouse cerebellar Purkinje cell survival

    Momoe Ishikawa, Tokiharu Sato, Hiroshi Kiyonari, Katsuji Yoshioka

    59   51 - 60   2015.1

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  • JSAP1とJLPによる軸索輸送の制御とその破綻がもたらす神経変性の分子機構 Invited

    佐藤時春, 石川桃絵, 善岡克次

    BioMedサーカス   2015

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    Authorship:Lead author  

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  • Impairment of cardiomyogenesis in embryonic stem cells lacking scaffold protein JSAP

    Sato T., Hidaka K., Iwanaga A., Ito M., Asano M., Nakabeppu Y., Morisaki T., Yoshioka Katsuji

    Cancer Research Institute report   2003   66 - 66   2006.3

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    Language:English  

    CiNii Article

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Industrial property rights

  • 情動障害の治療剤のスクリーニング方法

    善岡 克次, 吉原 亨, 佐藤 時春, 浅野 雅秀

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    Application no:特願2010-208662  Date applied:2010.9

    Announcement no:特開2011-089982 

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Awards

  • The 25th Annual Neuroscience Poster Session, 1st place prize

    2018.12  

    佐藤 時春

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Research Projects

  • 脳梗塞からの機能回復過程における時間的・空間的な病態の遷移プロセスの解明

    Grant number:21K07290

    2021.4 - 2025.3

    System name:科学研究費助成事業

    Research category:基盤研究(C)

    Awarding organization:日本学術振興会

    佐藤 時春

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    Grant amount:\4160000 ( Direct Cost: \3200000 、 Indirect Cost:\960000 )

    脳梗塞は神経回路機能の破綻を引き起こす。限定的ではあるものの、再編により代償性の回路が形成され、一定の機能回復を示す。しかし、脳梗塞は引き起こされる部位やその大きさは様々であるため、再編様式も複雑であることが予想される。そこで、本年度は、脳梗塞の起こる位置や大きさにより、皮質脊髄路がどのような再編パターンを示すのかを調べた。そのために、まず、マウスにおいて、皮質脊髄路の様々なタイプが位置するrostral forelimb area (RFA)、caudal forelimb area (CFA)、primary somatosensory cortex (S1)の大脳皮質領域で脳梗塞の位置や大きさを調節できる実験モデルを確立し、順行性トレーサーで皮質脊髄路をタイプ別に標識することで、軸索投射のパターンを詳細に解析、評価した。その結果、1. 広範囲な梗塞の場合、残存した対側の皮質脊髄路は再編を起こすこと、2. 障害領域が小さい場合、周囲の残存した同側の皮質脊髄路が再編に寄与すること、3. 運動野と感覚野のような機能的に異なった皮質脊髄路はお互いに再編による代償的な回路を形成しないという再編機序を見出した。

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  • Analysis of spatio-temporal gene expression patterns after brain injury

    Grant number:19K23773

    2019.8 - 2021.3

    System name:Grants-in-Aid for Scientific Research

    Research category:Grant-in-Aid for Research Activity Start-up

    Awarding organization:Japan Society for the Promotion of Science

    Sato Tokiharu

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    Grant amount:\2860000 ( Direct Cost: \2200000 、 Indirect Cost:\660000 )

    Brain injury damages neural circuits and severely impairs neural functions, however, spared neuronal circuit is often reorganized and partially recovers the functions. In the present study, we examined the gene expression patterns which regulate the process of neuronal reorganization. We revealed spatio-temporal gene expression patterns induced by the injury and neural activity that was evoked by rehabilitative training.

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Teaching Experience (researchmap)