Updated on 2025/09/04

写真a

 
IWAKURA Yuriko
 
Organization
Brain Research Institute Assistant Professor
Title
Assistant Professor
External link

Degree

  • 博士(医学) ( 2004.3   新潟大学 )

Research Interests

  • glutamate

  • EGF

  • NRG1

  • neurotrophic factor

  • monoamine

Research Areas

  • Life Science / Neuroscience-general

Research History (researchmap)

  • Niigata University   Brain Research Institute Basic Neuroscience Branch   Assistant Professor

    2007.2

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  • ニューヨーク大学スカボール研究所分子神経生物学分野   研究員

    2005.4 - 2007.1

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  • Niigata University   Brain Research Institute   Special researcher of the Japan Society for the Promotion of Science

    2003.4 - 2005.3

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Research History

  • Niigata University   Brain Research Institute Basic Neuroscience Branch   Assistant Professor

    2007.2

Education

  • Niigata University   Graduate School, Division of Medicine   生理系(分子神経生物学)

    - 2004.3

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    Country: Japan

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Professional Memberships

Committee Memberships

  • 日本神経科学学会   ダイバーシティ推進委員  

    2017.5 - 2019.5   

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    Committee type:Academic society

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  • 日本神経化学会   評議員  

    2013   

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    Committee type:Academic society

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Papers

  • Epidermal Growth Factor Suppresses the Development of GABAergic Neurons Via the Modulation of Perineuronal Net Formation in the Neocortex of Developing Rodent Brains. International journal

    Yuriko Iwakura, Yutaro Kobayashi, Hisaaki Namba, Hiroyuki Nawa, Nobuyuki Takei

    Neurochemical research   49 ( 5 )   1347 - 1358   2024.5

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    Previously, we reported that epidermal growth factor (EGF) suppresses GABAergic neuronal development in the rodent cortex. Parvalbumin-positive GABAergic neurons (PV neurons) have a unique extracellular structure, perineuronal nets (PNNs). PNNs are formed during the development of PV neurons and are mainly formed from chondroitin sulfate (CS) proteoglycans (CSPGs). We examined the effect of EGF on CSPG production and PNN formation as a potential molecular mechanism for the inhibition of inhibiting GABAergic neuronal development by EGF. In EGF-overexpressing transgenic (EGF-Tg) mice, the number of PNN-positive PV neurons was decreased in the cortex compared with that in wild-type mice, as in our previous report. The amount of CS and neurocan was also lower in the cortex of EGF-Tg mice, with a similar decrease observed in EGF-treated cultured cortical neurons. PD153035, an EGF receptor (ErbB1) kinase inhibitor, prevented those mentioned above excess EGF-induced reduction in PNN. We explored the molecular mechanism underlying the effect of EGF on PNNs using fluorescent substrates for matrix metalloproteinases (MMPs) and a disintegrin and metalloproteinases (ADAMs). EGF increased the enzyme activity of MMPs and ADAMs in cultured neurons. These enzyme activities were also increased in the EGF-Tg mice cortex. GM6001, a broad inhibitor of MMPs and ADAMs, also blocked EGF-induced PNN reductions. Therefore, EGF/EGF receptor signals may regulate PNN formation in the developing cortex.

    DOI: 10.1007/s11064-024-04122-y

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  • Cerebrocortical activation following unilateral labyrinthectomy in mice characterized by whole-brain clearing: implications for sensory reweighting. International journal

    Ryota Kai, Kuniyuki Takahashi, Kazuki Tainaka, Yuriko Iwakura, Hisaaki Namba, Nae Saito, Toshikuni Sasaoka, Shun Yamaguchi, Hiroyuki Nawa, Arata Horii

    Scientific reports   12 ( 1 )   15424 - 15424   2022.9

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    Posture and gait are maintained by sensory inputs from the vestibular, visual, and somatosensory systems and motor outputs. Upon vestibular damage, the visual and/or somatosensory systems functionally substitute by cortical mechanisms called "sensory reweighting". We investigated the cerebrocortical mechanisms underlying sensory reweighting after unilateral labyrinthectomy (UL) in mice. Arc-dVenus transgenic mice, in which the gene encoding the fluorescent protein dVenus is transcribed under the control of the promoter of the immediate early gene Arc, were used in combination with whole-brain three-dimensional (3D) imaging. Performance on the rotarod was measured as a behavioral correlate of sensory reweighting. Following left UL, all mice showed the head roll-tilt until UL10, indicating the vestibular periphery damage. The rotarod performance worsened in the UL mice from UL1 to UL3, which rapidly recovered. Whole-brain 3D imaging revealed that the number of activated neurons in S1, but not in V1, in UL7 was higher than that in sham-treated mice. At UL7, medial prefrontal cortex (mPFC) and agranular insular cortex (AIC) activation was also observed. Therefore, sensory reweighting to the somatosensory system could compensate for vestibular dysfunction following UL; further, mPFC and AIC contribute to the integration of sensory and motor functions to restore balance.

    DOI: 10.1038/s41598-022-19678-4

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  • Elevation of EGR1/zif268, a Neural Activity Marker, in the Auditory Cortex of Patients with Schizophrenia and its Animal Model International journal

    Yuriko Iwakura, Ryoka Kawahara-Miki, Satoshi Kida, Hidekazu Sotoyama, Ramil Gabdulkhaev, Hitoshi Takahashi, Yasuto Kunii, Mizuki Hino, Atsuko Nagaoka, Ryuta Izumi, Risa Shishido, Toshiyuki Someya, Hirooki Yabe, Akiyoshi Kakita, Hiroyuki Nawa

    Neurochemical Research   47 ( 9 )   2715 - 2727   2022.4

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:Springer Science and Business Media LLC  

    The family of epidermal growth factor (EGF) including neuregulin-1 are implicated in the neuropathology of schizophrenia. We established a rat model of schizophrenia by exposing perinatal rats to EGF and reported that the auditory pathophysiological traits of this model such as prepulse inhibition, auditory steady-state response, and mismatch negativity are relevant to those of schizophrenia. We assessed the activation status of the auditory cortex in this model, as well as that in patients with schizophrenia, by monitoring the three neural activity-induced proteins: EGR1 (zif268), c-fos, and Arc. Among the activity markers, protein levels of EGR1 were significantly higher at the adult stage in EGF model rats than those in control rats. The group difference was observed despite an EGF model rat and a control rat being housed together, ruling out the contribution of rat vocalization effects. These changes in EGR1 levels were seen to be specific to the auditory cortex of this model. The increase in EGR1 levels were detectable at the juvenile stage and continued until old ages but displayed a peak immediately after puberty, whereas c-fos and Arc levels were nearly indistinguishable between groups at all ages with an exception of Arc decrease at the juvenile stage. A similar increase in EGR1 levels was observed in the postmortem superior temporal cortex of patients with schizophrenia. The commonality of the EGR1 increase indicates that the EGR1 elevation in the auditory cortex might be one of the molecular signatures of this animal model and schizophrenia associating with hallucination.

    DOI: 10.1007/s11064-022-03599-9

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    Other Link: https://link.springer.com/article/10.1007/s11064-022-03599-9/fulltext.html

  • The dual role of dopamine in the modulation of information processing in the prefrontal cortex underlying social behavior. International journal

    Hidekazu Sotoyama, Hiroyoshi Inaba, Yuriko Iwakura, Hisaaki Namba, Nobuyuki Takei, Toshikuni Sasaoka, Hiroyuki Nawa

    FASEB journal : official publication of the Federation of American Societies for Experimental Biology   36 ( 2 )   e22160   2022.2

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    Dopamine in the prefrontal cortex is essential for the regulation of social behavior. However, stress-causing social withdrawal also promotes dopamine release in the prefrontal cortex. Thus, this evidence suggests opposite functions of dopamine in the prefrontal cortex. However, the influence of dopamine on prefrontal functions is yet to be fully understood. Here, we show that dopamine differentially modulated the neuronal activity triggered by social stimuli in the prefrontal cortex, depending on the duration of the dopamine activation (transient or sustained activation). Using chemogenetic techniques, we have found that social behavior was negatively regulated by a sustained increase in dopamine neuronal activity in the ventral tegmental area, while it was positively regulated by an acute increase. The duration of social interactions was positively correlated with the transient dopamine release triggered by social stimuli in the prefrontal cortex and negatively correlated with the sustained increase in prefrontal dopamine levels. Furthermore, the elevation of neural calcium signal, triggered by social stimuli, in the prefrontal cortex was attenuated by the persistent elevation of prefrontal dopamine levels, whereas an acute increase in dopamine levels enhanced it. Additionally, the chronic excess of dopamine suppressed c-Fos induction triggered by social stimuli in prefrontal neurons expressing dopamine D1 receptors, but not D2 receptors. These results suggest that sustained activation of prefrontal dopamine, at the opposite of its transient activation, can reduce prefrontal activity associated with social behavior, even for identical dopamine concentrations. Thus, dopamine plays opposite roles in modulating prefrontal activity depending on the duration of its action.

    DOI: 10.1096/fj.202101637R

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  • USP10 inhibits aberrant cytoplasmic aggregation of TDP-43 by promoting stress granule clearance. International journal

    Masahiko Takahashi, Hiroki Kitaura, Akiyoshi Kakita, Taichi Kakihana, Yoshinori Katsuragi, Osamu Onodera, Yuriko Iwakura, Hiroyuki Nawa, Masaaki Komatsu, Masahiro Fujii

    Molecular and cellular biology   42 ( 3 )   MCB0039321   2022.1

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    TDP-43 is a causative factor of amyotrophic lateral sclerosis (ALS). Cytoplasmic TDP-43 aggregates in neurons are a hallmark pathology of ALS. Under various stress conditions, TDP-43 localizes sequentially to two cytoplasmic protein aggregates: stress granules (SGs) first, and then aggresomes. Accumulating evidence suggests that delayed clearance of TDP-43-positive SGs is associated with pathological TDP-43 aggregates in ALS. We found that USP10 promotes the clearance of TDP-43-positive SGs in cells treated with proteasome inhibitor, thereby promoting the formation of TDP-43-positive aggresomes, and the depletion of USP10 increases the amount of insoluble TDP-35, a cleaved product of TDP-43, in the cytoplasm. TDP-35 interacted with USP10 in an RNA-binding dependent manner; however, impaired RNA-binding of TDP-35 reduced the localization in SGs and aggresomes and induced USP10-negative TDP-35 aggregates. Immunohistochemistry showed that most of the cytoplasmic TDP-43/TDP-35-aggregates in the neurons of ALS patients were USP10-negative. Our findings suggest that USP10 inhibits aberrant aggregation of TDP-43/TDP-35 in the cytoplasm of neuronal cells by promoting the clearance of TDP-43/TDP-35-positive SGs and facilitating the formation of TDP-43/TDP-35-positive aggresomes.

    DOI: 10.1128/MCB.00393-21

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  • Inter-breeder differences in prepulse inhibition deficits of C57BL/6J mice in a maternal infection model for schizophrenia International journal

    Yutaro Kobayashi, Hiroyoshi Inaba, Yuriko Iwakura, Hisaaki Namba, Hidekazu Sotoyama, Yui Murata, Kazuya Iwamoto, Hiroyuki Nawa

    Neuropsychopharmacology reports   41 ( 3 )   416 - 421   2020.12

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:Cold Spring Harbor Laboratory  

    <title>ABSTRACT</title>Genetic and environmental factors interact with each other to influence the risk of various psychiatric diseases; however, the intensity and nature of their interactions remain to be elucidated. We used a maternal infection model using polyinosinic-polycytidylic acid (Poly(I:C)) to determine the relationship between the maternal breeding environment and behavioral changes in the offspring. We purchased pregnant C57BL/6J mice from three breeders and administered Poly(I:C) (2 mg/kg) intravenously in their tail vein on gestation day 15. The offspring were raised to 8-12 weeks old and subjected to the acoustic startle tests to measure their startle response intensity, prepulse inhibition levels, and degree of the adaptation of the startle response. No statistical interaction between Poly(I:C) administration and sex was observed for prepulse inhibition; thus, male and female mice were analyzed together. The Poly(I:C) challenge significantly decreased prepulse inhibition levels of the offspring born to the pregnant dams from Breeder A but not those from the other breeders. However, there were no significant inter-breeder differences in Poly(I:C) effects on startle response and on startle adaptation. The rearing environment of mouse dams has a prominent impact on the Poly(I:C)-induced prepulse inhibition deficits in this maternal infection model.

    DOI: 10.1101/2020.12.24.423890

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  • Clozapine-dependent inhibition of EGF/neuregulin receptor (ErbB) kinases. Reviewed International journal

    Kobayashi Y, Iwakura Y, Sotoyama H, Kitayama E, Takei N, Someya T, Nawa H

    Translational psychiatry   9 ( 1 )   181 - 181   2019.8

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    Clozapine is an antipsychotic agent prescribed to psychotic patients exhibiting tolerance and/or resistance to the conventional antipsychotic medications that mainly drive monoamine antagonism. As the pharmacological fundamentals of its unique antipsychotic profile have been unrevealed, here, we attempted to obtain hints at this question. Here, we found that clozapine directly acts on ErbB kinases to downregulate epidermal growth factor (EGF)/neuregulin signaling. In cultured cell lines and cortical neurons, EGF-triggered ErbB1 phosphorylation was diminished by 30 μM clozapine, but not haloperidol, risperidone, or olanzapine. The neuregulin-1-triggered ErbB4 phosphorylation was attenuated by 10 μM clozapine and 30 μM haloperidol. We assumed that clozapine may directly interact with the ErbB tyrosine kinases and affect their enzyme activity. To test this assumption, we performed in vitro kinase assays using recombinant truncated ErbB kinases. Clozapine (3-30 μM) significantly decreased the enzyme activity of the truncated ErbB1, B2, and B4 kinases. Acute in vivo administration of clozapine (20 mg/kg) to adult rats significantly suppressed the basal phosphorylation levels of ErbB4 in the brain, although we failed to detect effects on basal ErbB1 phosphorylation. Altogether with the previous findings that quinazoline inhibitors for ErbB kinases harbor antipsychotic potential in animal models for schizophrenia, our present observations suggest the possibility that the micromolar concentrations of clozapine can attenuate the activity of ErbB receptor kinases, which might illustrate a part of its unique antipsychotic psychopharmacology.

    DOI: 10.1038/s41398-019-0519-1

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    Other Link: http://www.nature.com/articles/s41398-019-0519-1

  • USP10 is a critical factor for Tau-positive stress granule formation in neuronal cells. Reviewed International journal

    Piatnitskaia S, Takahashi M, Kitaura H, Katsuragi Y, Kakihana T, Zhang L, Kakita A, Iwakura Y, Nawa H, Miura T, Ikeuchi T, Hara T, Fujii M

    Scientific reports   9 ( 1 )   10591 - 10591   2019.7

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    Tau aggregates in neurons of brain lesions is a hallmark pathology of tauopathies, including Alzheimer's disease (AD). Recent studies suggest that the RNA-binding protein TIA1 initiates Tau aggregation by inducing the formation of stress granules (SGs) containing Tau. SGs are stress-inducible cytoplasmic protein aggregates containing many RNA-binding proteins that has been implicated as an initial site of multiple pathogenic protein aggregates in several neurodegenerative diseases. In this study, we found that ubiquitin-specific protease 10 (USP10) is a critical factor for the formation of Tau/TIA1/USP10-positive SGs. Proteasome inhibition or TIA1-overexpression in HT22 neuronal cells induced the formation of TIA1/Tau-positive SGs, and the formations were severely attenuated by depletion of USP10. In addition, the overexpression of USP10 without stress stimuli in HT22 cells induced TIA1/Tau/USP10-positive SGs in a deubiquitinase-independent manner. In AD brain lesions, USP10 was colocalized with Tau aggregates in the cell body of neurons. The present findings suggest that USP10 plays a key role in the initiation of pathogenic Tau aggregation in AD through SG formation.

    DOI: 10.1038/s41598-019-47033-7

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  • 統合失調症患者における脳内コンドロイチン硫酸鎖の変化

    湯川 尊行, 岩倉 百合子, 武井 延之, 斎藤 摩美, 渡部 雄一郎, 豊岡 和彦, 五十嵐 道弘, 新里 和弘, 大島 健一, 國井 泰人, 矢部 博興, 松本 純弥, 和田 明, 日野 瑞城, 入谷 修司, 丹羽 真一, 竹内 亮子, 高橋 均, 柿田 明美, 染矢 俊幸, 那波 宏之

    精神神経学雑誌   ( 2019特別号 )   S410 - S410   2019.6

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    Language:Japanese   Publisher:(公社)日本精神神経学会  

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  • Pathological alterations of chondroitin sulfate moiety in postmortem hippocampus of patients with schizophrenia. Reviewed International journal

    Yukawa T, Iwakura Y, Takei N, Saito M, Watanabe Y, Toyooka K, Igarashi M, Niizato K, Oshima K, Kunii Y, Yabe H, Matsumoto J, Wada A, Hino M, Iritani S, Niwa SI, Takeuchi R, Takahashi H, Kakita A, Someya T, Nawa H

    Psychiatry research   270   940 - 946   2018.12

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    Perineuronal nets comprise chondroitin sulfate moieties and their core proteins, and their neuropathological alterations have been implicated in schizophrenia. To explore the molecular mechanism of the perineuronal net impairments in schizophrenia, we measured the immunoreactivity of chondroitin sulfate moieties, major components of perineuronal nets, in three brain regions (postmortem dorsolateral prefrontal cortex, caudate nucleus, and hippocampus) of schizophrenia patients and control subjects. Immunoblotting for chondroitin 4-sulfate and chondroitin 6-sulfate moieties revealed a significant increase in intensity of a 180 kD band of chondroitin 4-sulfate immunoreactivity in the hippocampus of patients, although we detected no significant alteration in their immunoreactivities with any other molecular sizes or in other brain regions. The levels of immunoreactivity were not correlated with postmortem interval, age, or storage time. We failed to find such an increase in a similar molecular range of the chondroitin 4-sulfate immunoreactivity in the hippocampus of the rats chronically treated with haloperidol. These results suggest that the level alteration of the chondroitin 4-sulfate moiety might contribute to the perineuronal net abnormality found in patients with schizophrenia.

    DOI: 10.1016/j.psychres.2018.10.062

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  • USP10 Is a Driver of Ubiquitinated Protein Aggregation and Aggresome Formation to Inhibit Apoptosis. Reviewed International journal

    Takahashi M, Kitaura H, Kakita A, Kakihana T, Katsuragi Y, Nameta M, Zhang L, Iwakura Y, Nawa H, Higuchi M, Komatsu M, Fujii M

    iScience   9   433 - 450   2018.11

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    Accumulation of ubiquitinated proteins is cytotoxic, but cells inactivate these cytotoxicities by inducing aggresome formation. We found that ubiquitin-specific protease 10 (USP10) inhibits ubiquitinated protein-induced apoptosis by inducing aggresome formation. USP10 interacted with the ubiquitin receptor p62 and the interaction augmented p62-dependent ubiquitinated protein aggregation and aggresome formation, thereby cooperatively inhibiting apoptosis. We provide evidence that USP10/p62-induced protein aggregates inhibit proteasome activity, which increases the amount of ubiquitinated proteins and promotes aggresome formation. USP10 induced aggresomes containing α-synuclein, a pathogenic protein in Parkinson disease, in cultured cells. In Parkinson disease brains, USP10 was colocalized with α-synuclein in the disease-linked aggresome-like inclusion Lewy bodies, suggesting that USP10 inhibits α-synuclein-induced neurotoxicity by promoting Lewy body formation. Collectively, these findings suggest that USP10 is a critical factor to control protein aggregation, aggresome formation, and cytotoxicity in protein-aggregation-related diseases.

    DOI: 10.1016/j.isci.2018.11.006

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  • Epidermal growth factor signals attenuate phenotypic and functional development of neocortical GABA neurons Reviewed International journal

    Hisaaki Namba, Tadasato Nagano, Eiichi Jodo, Satoshi Eifuku, Masao Horie, Hirohide Takebayashi, Yuriko Iwakura, Hidekazu Sotoyama, Nobuyuki Takei, Hiroyuki Nawa

    Journal of Neurochemistry   142 ( 6 )   886 - 900   2017.9

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:Blackwell Publishing Ltd  

    DOI: 10.1111/jnc.14097

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  • Epidermal growth factor singals attenuate phenotypic and functional development of neocortical GABA neurons Reviewed

    Hisaaki Namba, Tadasato Nagano, Eiichi Jodo, Satoshi Eifuku, Masao Horie, Hirohide Takebayashi, Yuriko Iwakura, Hidekazu Sotoyama, Nobuyuki Takei, Hiroyuki Nawa

    JOURNAL OF NEUROCHEMISTRY   142 ( 6 )   886 - 900   2017.9

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    DOI: 10.1111/jnc.14097

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  • Striatal hypodopamine phenotypes found in transgenic mice that overexpress glial cell line-derived neurotrophic factor Reviewed International journal

    Hidekazu Sotoyama, Yuriko Iwakura, Kanako Oda, Toshikuni Sasaoka, Nobuyuki Takei, Akiyoshi Kakita, Hideki Enomoto, Hiroyuki Nawa

    NEUROSCIENCE LETTERS   654 ( 654 )   99 - 106   2017.7

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    DOI: 10.1016/j.neulet.2017.06.005

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  • Advanced Glycation End Products Induce Brain-Derived Neurotrophic Factor Release from Human Platelets through the Src Family Kinases Activation Reviewed

    Furukawa Kazuo, Fuse Ichiro, Iwakura Yuriko, Sotoyama Hidekazu, Hanyu Osamu, Nawa Hiroyuki, Takei Nobuyuki, Sone Hirohito

    DIABETES   66   A123   2017.6

  • Glutamate-dependent ectodomain shedding of neuregulin-1 type II precursors in rat forebrain neurons Reviewed International journal

    Yuriko Iwakura, Ran Wang, Naoko Inamura, Kazuaki Araki, Shigeki Higashiyama, Nobuyuki Takei, Hiroyuki Nawa

    PLOS ONE   12 ( 3 )   e0174780   2017.3

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    DOI: 10.1371/journal.pone.0174780

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  • Advanced glycation end products induce brain-derived neurotrophic factor release from human platelets through the Src-family kinase activation Reviewed International journal

    Kazuo Furukawa, Ichiro Fuse, Yuriko Iwakura, Hidekazu Sotoyama, Osamu Hanyu, Hiroyuki Nawa, Hirohito Sone, Nobuyuki Takei

    CARDIOVASCULAR DIABETOLOGY   16 ( 1 )   20 - 20   2017.2

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    DOI: 10.1186/s12933-017-0505-y

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  • Level of plasma neuregulin-1 SMDF is reduced in patients with idiopathic Parkinson's disease Reviewed International journal

    Yuka Hama, Ichiro Yabe, Koichi Wakabayashi, Takahiro Kano, Makoto Hirotani, Yuriko Iwakura, Jun Utsumi, Hidenao Sasaki

    NEUROSCIENCE LETTERS   587 ( 587 )   17 - 21   2015.2

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    DOI: 10.1016/j.neulet.2014.12.024

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  • Neurobehavioral Differences Between Mice Receiving Distinct Neuregulin Variants as Neonates; Impact on Sensitivity to MK-801 Reviewed

    T. Kato, Y. Abe, S. Hirokawa, Y. Iwakura, M. Mizuno, H. Namba, H. Nawa

    CURRENT MOLECULAR MEDICINE   15 ( 3 )   222 - 236   2015

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  • Neuropathologic implication of peripheral neuregulin-1 and EGF signals in dopaminergic dysfunction and behavioral deficits relevant to schizophrenia: Their target cells and time window Reviewed International journal

    Hiroyuki Nawa, Hidekazu Sotoyama, Yuriko Iwakura, Nobuyuki Takei, Hisaaki Namba

    BioMed Research International   2014 ( 2014 )   697935 - 697935   2014

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:Hindawi Publishing Corporation  

    DOI: 10.1155/2014/697935

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  • Neurobehavioral deficits of epidermal growth factor-overexpressing transgenic mice: impact on dopamine metabolism. Reviewed International journal

    Eda Takeyoshi, Mizuno Makoto, Araki Kazuaki, Iwakura Yuriko, Namba Hisaaki, Sotoyama Hidekazu, Kakita Akiyoshi, Takahashi Hitoshi, Satoh Hiroshi, Chan Siu-Yuen, Nawa Hiroyuki

    Neurosci Lett   547   21 - 25   2013.6

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    Epidermal growth factor (EGF) and its family member neuregulin-1 are implicated in the etiology of schizophrenia. Our recent pharmacological studies indicate that EGF injections to neonatal and adult rats both induce neurobehavioral deficits relevant to schizophrenia. We, however, did not evaluate the genetic impact of EGF transgene on neurobehavioral traits. Here we analyzed transgenic mice carrying the transgene of mouse EGF cDNA. As compared to control littermates, heterozygous EGF transgenic mice had an increase in EGF mRNA levels and showed significant decreases in prepulse inhibition and context-dependent fear learning, but there were no changes in locomotor behaviors and sound startle responses. In addition, these transgenic mice exhibited higher behavioral sensitivity to the repeated cocaine injections. There were neurochemical alterations in metabolic enzymes of dopamine (i.e., tyrosine hydroxylase, dopa decarboxylase, catechol-O-methyl transferase) and monoamine contents in various brain regions of the EGF transgenic mice, but there were no apparent neuropathological signs in the brain. The present findings rule out the indirect influence of anti-EGF antibody production

    DOI: 10.1016/j.neulet.2013.04.055

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  • Neurobehavioral deficits of epidermal growth factor-overexpressing transgenic mice: Impact on dopamine metabolism Reviewed

    Takeyoshi Eda, Makoto Mizuno, Kazuaki Araki, Yuriko Iwakura, Hisaaki Namba, Hidekazu Sotoyama, Akiyoshi Kakita, Hitoshi Takahashi, Hiroshi Satoh, Siu-Yuen Chan, Hiroyuki Nawa

    NEUROSCIENCE LETTERS   547 ( 547 )   21 - 25   2013.6

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    DOI: 10.1016/j.neulet.2013.04.055

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  • ErbB inhibitors ameliorate behavioral impairments of an animal model for schizophrenia: implication of their dopamine-modulatory actions Reviewed

    M. Mizuno, H. Sotoyama, H. Namba, M. Shibuya, T. Eda, R. Wang, T. Okubo, K. Nagata, Y. Iwakura, H. Nawa

    TRANSLATIONAL PSYCHIATRY   3 ( 3 )   e252   2013.4

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    DOI: 10.1038/tp.2013.29

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  • ErbB2 dephosphorylation and anti-proliferative effects of neuregulin-1 in ErbB2-overexpressing cells; re-evaluation of their low-affinity interaction. Reviewed International journal

    Wang Ran, Iwakura Yuriko, Araki Kazuaki, Keino-Masu Kazuko, Masu Masayuki, Wang Xue-yi, Takei Nobuyuki, Higashiyama Shigeki, Nawa Hiroyuki

    Sci Rep   3   1402 - 1402   2013.3

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    DOI: 10.1038/srep01402

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  • ErbB2 dephosphorylation and anti-proliferative effects of neuregulin-1 in erbb2-overexpressing cells; Re-evaluation of their low-affinity interaction Reviewed

    Ran Wang, Yuriko Iwakura, Kazuaki Araki, Kazuko Keino-Masu, Masayuki Masu, Xue-Yi Wang, Nobuyuki Takei, Shigeki Higashiyama, Hiroyuki Nawa

    Scientific Reports   3 ( 3 )   1402   2013

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    DOI: 10.1038/srep01402

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  • ErbB1-4-dependent EGF/neuregulin signals and their cross talk in the central nervous system: Pathological implications in schizophrenia and Parkinson's disease Reviewed International journal

    Yuriko Iwakura, Hiroyuki Nawa

    Frontiers in Cellular Neuroscience   13 ( 2013 )   1 - 35   2013

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    DOI: 10.3389/fncel.2013.00004

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  • Pallidalhyperdopaminergic innervation induced by neonatal exposure to epidermal growth factor; implication in schizophrenia Reviewed

    Nawa H, Namba H, Iwakura Y, Takei N, Sotoyama H

    JOURNAL OF NEUROCHEMISTRY   123   20   2012.10

  • Pallidal Hyperdopaminergic Innervation Underlying D2 Receptor-Dependent Behavioral Deficits in the Schizophrenia Animal Model Established by EGF Reviewed International journal

    Hidekazu Sotoyama, Yingjun Zheng, Yuriko Iwakura, Makoto Mizuno, Miho Aizawa, Ksenia Shcherbakova, Ran Wang, Hisaaki Namba, Hiroyuki Nawa

    PLOS ONE   6 ( 10 )   e25831   2011.10

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    DOI: 10.1371/journal.pone.0025831

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  • Dopamine-dependent ectodomain shedding and release of epidermal growth factor in developing striatum: target-derived neurotrophic signaling (Part 2) Reviewed International journal

    Yuriko Iwakura, Ran Wang, Yuichi Abe, Ying-shan Piao, Yuji Shishido, Shigeki Higashiyama, Nobuyuki Takei, Hiroyuki Nawa

    JOURNAL OF NEUROCHEMISTRY   118 ( 1 )   57 - 68   2011.7

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    DOI: 10.1111/j.1471-4159.2011.07295.x

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  • Qualitative and quantitative re-evaluation of epidermal growth factor-ErbB1 action on developing midbrain dopaminergic neurons in vivo and in vitro: target-derived neurotrophic signaling (Part 1) Reviewed International journal

    Yuriko Iwakura, Yingjun Zheng, Maria Sibilia, Yuichi Abe, Ying-shan Piao, Daisaku Yokomaku, Ran Wang, Yuta Ishizuka, Nobuyuki Takei, Hiroyuki Nawa

    JOURNAL OF NEUROCHEMISTRY   118 ( 1 )   45 - 56   2011.7

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    DOI: 10.1111/j.1471-4159.2011.07287.x

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  • In vitro production of an active neurotrophic factor, neuregulin-1: Qualitative comparison of different cell-free translation systems Reviewed International journal

    Ran Wang, Yuriko Iwakura, Kazuaki Araki, Hidekazu Sotoyama, Nobuyuki Takei, Hiroyuki Nawa

    NEUROSCIENCE LETTERS   497 ( 2 )   90 - 93   2011.6

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    DOI: 10.1016/j.neulet.2011.04.036

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  • Neuregulin-1 Signals from the Periphery Regulate AMPA Receptor Sensitivity and Expression in GABAergic Interneurons in Developing Neocortex Reviewed International journal

    Yuichi Abe, Hisaaki Namba, Taisuke Kato, Yuriko Iwakura, Hiroyuki Nawa

    JOURNAL OF NEUROSCIENCE   31 ( 15 )   5699 - 5709   2011.4

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    DOI: 10.1523/JNEUROSCI.3477-10.2011

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  • Regulated processing/release of neuregulin-1 precursors in rat cortical neurons Reviewed

    Iwakura Yuriko, Wang Ran, Araki Kazuaki, Nawa Hiroyuki

    NEUROSCIENCE RESEARCH   71   E138   2011

  • Antipsychotic Potential of Quinazoline ErbB1 Inhibitors in a Schizophrenia Model Established With Neonatal Hippocampal Lesioning Reviewed

    Makoto Mizuno, Yuriko Iwakura, Masako Shibuya, Yingjun Zheng, Takeyoshi Eda, Taisuke Kato, Yohei Takasu, Hiroyuki Nawa

    JOURNAL OF PHARMACOLOGICAL SCIENCES   114 ( 3 )   320 - 331   2010.11

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    DOI: 10.1254/jphs.10099FP

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  • Distinct ErbB receptor binding and signaling of neuregulin-1 splicing isoforms Reviewed

    Wang Ran, Iwakura Yuriko, Takei Nobuyuki, Ishizuka Yuta, Zheng Yingjun, Kato Taisuke, Higashiyama Shigeki, Nawa Hiroyuki

    NEUROSCIENCE RESEARCH   68   E142   2010

  • Molecular pathology of ErbB signaling in schizophrenia and its models Reviewed

    Nawa Hiroyuki, Mizuno Makoto, Sotoyama Hidekazu, Zheng Yingjun, Kato Taisuke, Abe Yuichi, Sakai Miwako, Shibuya Masako, Eda Takeyoshi, Wang Ran, Araki Kazuaki, Ishizuka Yuta, Takei Nobuyuki, Iwakura Yuriko, Namba Hisaaki

    NEUROSCIENCE RESEARCH   65   S31   2009

  • Dopamine D1 receptor-induced signaling through TrkB receptors in striatal neurons Reviewed International journal

    Yuriko Iwakura, Hiroyuki Nawa, Ichiro Sora, Moses V. Chao

    JOURNAL OF BIOLOGICAL CHEMISTRY   283 ( 23 )   15799 - 15806   2008.6

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    DOI: 10.1074/jbc.M801553200

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  • Neurotrophic effects of EGF/ErbB1 signals on developing midbrain dopaminergic neurons Reviewed

    Iwakura Yuriko, Zheng Ying, Piao Ying-Shan, Yokomaku Daisaku, Aoki Hiroyuki, Takei Nobuyuki, Nawa Hiroyuki

    NEUROSCIENCE RESEARCH   58   S58   2007

  • Transforming growth factor alpha attenuates the functional expression of AMPA receptors in cortical GABAergic neurons Reviewed International journal

    H Namba, T Nagano, Y Iwakura, H Xiong, H Jourdi, N Takei, H Nawa

    MOLECULAR AND CELLULAR NEUROSCIENCE   31 ( 4 )   628 - 641   2006.4

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    DOI: 10.1016/j.mcn.2005.12.002

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  • Intereukin-1 receptor antagonist effects on neural and behavioral development in mice Reviewed

    Tsuda N, Iwakura Y, Nawa H

    JOURNAL OF PHARMACOLOGICAL SCIENCES   100   144P   2006

  • Differential distributions of peptides in the epidermal growth factor family and phosphorylation of ErbB1 receptor in adult rat brain Reviewed International journal

    YS Piao, Y Iwakura, N Takei, H Nawa

    NEUROSCIENCE LETTERS   390 ( 1 )   21 - 24   2005.12

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    DOI: 10.1016/j.neulet.2005.07.048

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  • ErbB1 Ligands stimulate development of midbrain dopamine neurons; implications in schizophrenia.

    Iwakura Yuriko, Piao Ying-shan, Kim Seon howa, Watanabe Yuichiro, Nawa Hiroyuki

    Annunal Report of Mitsubishi Pharma Research Foundation   37 ( 37 )   138 - 143   2005.12

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  • Influences of dopaminergic lesion on epidermal growth factor-ErbB signals in Parkinson's disease and its model: neurotrophic implication in nigrostriatal neurons Reviewed International journal

    Y Iwakura, YS Piao, M Mizuno, N Takei, A Kakita, H Takahashi, H Nawa

    JOURNAL OF NEUROCHEMISTRY   93 ( 4 )   974 - 983   2005.5

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    DOI: 10.1111/j.1471-4159.2005.03073.x

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  • Regulated release of EGF-like molecules from rat striatal culture: Their trophic activity on midbrain dopaminergic neurons. Reviewed

    Iwakura Y, Piao YS, Takei N, Nawa H

    FASEB JOURNAL   18 ( 8 )   C255   2004.5

  • Brain-derived neurotrophic factor signal enhances and maintains the expression of AMPA receptor-associated PDZ proteins in developing cortical neurons Reviewed International journal

    H Jourdi, Y Iwakura, M Narisawa-Saito, K Ibaraki, HB Xiong, M Watanabe, Y Hayashi, N Takei, H Nawa

    DEVELOPMENTAL BIOLOGY   263 ( 2 )   216 - 230   2003.11

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    DOI: 10.1016/j.ydbio.2003.07.008

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  • Brain-derived neurotrophic factor regulates surface expression of alpha-amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid receptors by enhancing the N-ethylmaleimide-sensitive factor/GluR2 interaction in developing neocortical neurons Reviewed International journal

    M Narisawa-Saito, Y Iwakura, M Kawamura, K Araki, S Kozaki, N Takei, H Nawa

    JOURNAL OF BIOLOGICAL CHEMISTRY   277 ( 43 )   40901 - 40910   2002.10

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    DOI: 10.1074/jbc.M202158200

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  • N-methyl-D-aspartate-induced α -amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid (AMPA) receptor down-regulation involves interaction of the carboxyl terminus of GluR2/3 with Pick1: Ligand-binding studies using Sindbis vectors carrying AMPA receptor decoys Reviewed

    Yuriko Iwakura, Tadasato Nagano, Meiko Kawamura, Hiroshi Horikawa, Kyoko Ibaraki, Nobuyuki Takei, Hiroyuki Nawa

    Journal of Biological Chemistry   276 ( 43 )   40025 - 40032   2001.10

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    DOI: 10.1074/jbc.M103125200

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  • N-methyl-D-aspartate-induced alpha-amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid (AMPA) receptor down-regulation involves interaction of the carboxyl terminus of GluR2/3 with Pick1. Ligand-binding studies using Sindbis vectors carrying AMPA receptor

    Iwakura Y, Nagano T, Kawamura M, Horikawa H, Ibaraki K, Takei N, Nawa H

    J Biol Chem   276 ( 43 )   40025 - 40032   2001.10

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    The dynamics of alpha-amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid (AMPA)-type glutamate receptors, as represented by their exocytosis, endocytosis and cytoskeletal linkage, has often been implicated in N-methyl-d-aspartate (NMDA)-dependent synaptic plasticity. To explore the molecular mechanisms underlying the AMPA receptor dynamics, cultured hippocampal neurons were stimulated with 100 microm NMDA, and the biochemical and pharmacological changes in the ligand binding activity of AMPA receptor complexes and its subunits, GluR1 and GluR2/3, were investigated. The NMDA treatment reduced the total amount of bound [(3)H]AMPA on the surface of the neurons but not in their total membrane fraction. This process was mimicked by a protein kinase C activator, phorbol ester, but blocked by an inhibitor of the same kinase, calphostin C. The NMDA-induced down-regulation of the ligand binding activity was also reflected by the decreased AMPA-triggered channel activity as well as by the cells&#039; reduced immunoreactivity for GluR1. In parallel, the NMDA treatment markedly altered the interaction between the AMPA receptor subunits and their associating molecule(s); the association of PDZ m

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  • NMDA-induced AMPA receptor Down-regulation Requires Interaction of Carboxyl Terminus of GluR2/3 With Pick1

    Iwakura Y, Nagano T, Kawakura M, Horikawa H, Ibaraki K, Takei N, Nawa H

    Jounal of biological chemistry   2001.10

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  • Phenotypic down-regulation of glutamate receptor subunit GluR1 in Alzheimer's diseases Reviewed

    K Wakabayashi, M Narisawa-Saito, Y Iwakura, T Arai, K Ikeda, H Takahashi, H Nawa

    NEUROBIOLOGY OF AGING   20 ( 3 )   287 - 295   1999.5

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    DOI: 10.1016/S0197-4580(99)00035-4

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  • 統合失調症患者とそのモデル動物の聴覚野におけるEGR1/zif268の発現変化

    岩倉百合子, 岩倉百合子, 川原玲香, 喜田聡, 喜田聡, 外山英和, GABDULKHAEV Ramil, 高橋均, 國井泰人, 國井泰人, 日野瑞城, 日野瑞城, 長岡敦子, 泉竜太, 宍戸理紗, 染矢俊幸, 矢部博興, 柿田明美, 那波宏之, 那波宏之

    日本神経化学会大会抄録集(Web)   65th   2022

  • 統合失調症患者における脳内コンドロイチン硫酸鎖の変化

    湯川 尊行, 岩倉 百合子, 武井 延之, 斎藤 摩美, 渡部 雄一郎, 豊岡 和彦, 五十嵐 道弘, 新里 和弘, 大島 健一, 國井 泰人, 矢部 博興, 松本 純弥, 和田 明, 日野 瑞城, 入谷 修司, 丹羽 真一, 竹内 亮子, 高橋 均, 柿田 明美, 染矢 俊幸, 那波 宏之

    精神神経学雑誌   ( 2019特別号 )   S410 - S410   2019.6

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  • 最終糖化産物(AGEs)はヒト血小板において、Srcファミリーキナーゼの活性化を介して脳由来神経栄養因子(BDNF)の放出を促進させる

    古川 和郎, 布施 一郎, 岩倉 百合子, 外山 英和, 羽入 修, 那波 宏之, 曽根 博仁, 武井 延之

    生命科学系学会合同年次大会   2017年度   [2P - 1016]   2017.12

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  • 最終糖化産物(AGEs)はヒト血小板において、Srcファミリーキナーゼの活性化を介して脳由来神経栄養因子(BDNF)の放出を促進させる

    古川 和郎, 布施 一郎, 岩倉 百合子, 外山 英和, 羽入 修, 那波 宏之, 曽根 博仁, 武井 延之

    生命科学系学会合同年次大会   2017年度   [2P - 1016]   2017.12

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  • 最終糖化産物(AGE)はヒト血小板からSrc family kinaseの活性を介してBDNFの放出を促進させる

    古川 和郎, 武井 延之, 岩倉 百合子, 外山 英和, 羽入 修, 布施 一郎, 那波 宏之, 曽根 博仁

    糖尿病   59 ( Suppl.1 )   S - 309   2016.4

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  • セロトニン神経細胞の発達・成熟に対する選択的な栄養因子シグナルの作用機序の解明

    岩倉 百合子, 那波 宏之

    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   [2P1334] - [2P1334]   2015.12

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  • 線条体—黒質経路におけるドパミンと上皮成長因子(EGF)とのクロストーク Invited

    岩倉百合子

    神経化学   51 ( 3 )   59 - 64   2014.12

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  • ErbB1-4-dependent EGF/neuregulin signals and their cross talk in the central nervous system: pathological implications in schizophrenia and Parkinson's disease Invited Reviewed

    Yuriko Iwakura, Hiroyuki Nawa

    FRONTIERS IN CELLULAR NEUROSCIENCE   7   2013.2

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    DOI: 10.3389/fncel.2013.00004

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  • ニューレグリンとモノアミン伝達の相互作用

    岩倉 百合子

    上原記念生命科学財団研究報告集   26   1 - 5   2012.12

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  • ニューレグリン1タイプ1・2・3のErbB受容体結合差(Distinct receptor affinities of neuregulin-1 splicing variants to ErbB3 and ErbB4)

    王 冉, 岩倉 百合子, 武井 延之, 那波 宏之

    神経化学   50 ( 2-3 )   193 - 193   2011.9

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  • 神経栄養因子暴露に対するドーパミン神経回路発達の脆弱性 統合失調症との関連

    那波 宏之, 水野 誠, 加藤 泰介, 阿部 佑一, 坂井 美和子, 澁谷 雅子, 江田 岳, 王 冉, 荒木 一明, 石塚 佑太, 武井 延之, 岩倉 百合子, 難波 寿明, 外山 英和

    生化学   82 ( 9 )   883 - 883   2010.9

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  • モデル動物を用いた精神疾患のメカニズム研究 脳発達の視点から 末梢性サイトカインによるドーパミン神経回路発達の脆弱性と統合失調症

    那波 宏之, 外山 英和, 水野 誠, 加藤 泰介, 岩倉 百合子, 武井 延之, 難波 寿明

    日本臨床精神神経薬理学会・日本神経精神薬理学会合同年会プログラム・抄録集   20回・40回   53 - 53   2010.9

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  • ニューレグリン1亜型の示すErbB受容体親和性差とシグナル変化(Distinct ErbB receptor binding and signaling of neuregulin-1 splicing isoforms)

    王 冉, 岩倉 百合子, 武井 延之, 石塚 佑太, 鄭 英君, 加藤 泰介, 東山 繁樹, 那波 宏之

    神経化学   49 ( 2-3 )   544 - 544   2010.8

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  • 霊長類を用いた精神神経疾患モデルの現況と展望 上皮成長因子受容体リガンドを用いた統合失調症モデル動物(Schizophrenia animal models established with ErbB receptor ligands)

    那波 宏之, 水野 誠, 外山 英和, 鄭 英君, 加藤 泰介, 阿部 佑一, 坂井 美和子, 渋谷 雅子, 江田 岳誉, 王 冉, 荒木 一明, 石塚 佑太, 武井 延之, 岩倉 百合子, 難波 寿明

    神経化学   48 ( 2-3 )   184 - 184   2009.6

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  • 線条体神経細胞におけるTrkB受容体を介したドーパミンD1受容体誘発シグナル伝達(Dopamine D1 receptor-induced signaling through TrkB receptors in striatal neurons)

    岩倉 百合子, 那波 宏之, 曽良 一郎, チャオ V.・モーゼス

    神経化学   47 ( 2-3 )   230 - 230   2008.8

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  • Promoting action of endogenous and exogenous epidermal growth factor-ErbB1 signals on the development of midbrain dopaminergic neurons

    Zheng Yingjun, Iwakura Yuriko, Namba Hisaaki, Takei Nobuyuki, Sano Hiromi, Kobayashi Kazuto, Nawa Hiroyuki

    Proceedings of Annual Meeting of the Physiological Society of Japan   2006   172 - 172   2006

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    Epidermal growth factor (EGF) binds to ErbB1 receptor and exerts a neurotrophic activity on midbrain dopaminergic neurons. Here, using EGF administrated animals and midbrain cultures, we investigated endogenous and exogenous ErbB1 activity on the development of dopaminergic neurons. Immunostaining of tyrosine hydroxylase (TH) revealed that the chronic administration of ErbB1 inhibitors (PD153035, ZD1839) to rat neonates prevented dopaminergic neurons from axonal fiber outgrowth and striatal innervation. Further, protein levels of TH and dopamine transporter decreased in the striatum but did not change in the frontal cortex. In midbrain culture, EGF had promoting activities in cell-survival and dopamine uptake. To monitor the development of intrinsic excitability of the dopaminergic neurons we prepared midbrain cultures from TH-EGFP transgenic mice. Whole-cell current-clamp recording from EGFP positive dopaminergic cells revealed that chronic treatment with EGF increased the number of action potentials induced by current injections. Further, daily administrations of EGF in vivo increased AMPA-mediated synaptic responses in the dopaminergic neurons. These findings suggest that ErbB1 ligands such as EGF have a neurotrophic activity for the development of midbrain dopaminergic neurons. <b>[J Physiol Sci. 2006;56 Suppl:S172]</b>

    DOI: 10.14849/psjproc.2006.0.172.1

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  • 統合失調症の分子病態 EGFとIL-1はドーパミン性ニューロンに対し神経栄養活性を示すが後に認識異常を起こす(Neurotrophic activity of EGF and IL-1 on dopaminergic neurons and later cognitive abnormalities)

    那波 宏之, 岩倉 百合子, 水野 誠, 津田 法子, 鄭 英君, 渡部 雄一郎, 染矢 俊幸

    神経化学   44 ( 2-3 )   172 - 172   2005.8

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  • 成熟ラット脳における上皮細胞増殖因子ファミリーとリン酸化ErbB1の異なった分布(Differential Distributions of Epidermal Growth Factor Family and Phosphorylated ErbB1 in adult Rat Brain)

    朴 英善, 小見 笑子, 岩倉 百合子, 武井 延之, 那波 宏之

    神経化学   44 ( 2-3 )   227 - 227   2005.8

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  • ErbB1 Ligands stimulate development of midbrain dopamine neurons; implications in schizophrenia Invited

    Iwakura Y, Piao Y, Sotoyama H, Watanabe Y, Kim SH, Mizuno M, Nawa H

    Annual Reports of Mitsubishi Pharma Foundation   ( 37 )   138   2005

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  • パーキンソン病線条体におけるEGF/EGFレセプターシグナルの変化(Decreased EGF/ErbB1 receptor signal in the brain of patients with Parkinsons disease)

    岩倉 百合子, 柿田 明美, 朴 英善, 武井 延之, 那波 宏之

    神経化学   43 ( 2-3 )   529 - 529   2004.8

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  • ラット線条体初代培養神経細胞におけるEGFファミリー分子の放出調節(Regulated Release of EGF-like Molecules from Rat Striatal Culture: Their Trophic Activity on Midbrain Dopaminergic Neurons.)

    岩倉 百合子, 朴 英善, 武井 延之, 那波 宏之

    神経化学   42 ( 2-3 )   346 - 346   2003.8

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  • 神経活動に依存したEGF family分子のシェディング(Activity-dependent shedding of EGF family molecules in CNS)

    宍戸 裕二, 田中 隆之, 岩倉 百合子, 東山 繁樹, 武井 延之, 那波 宏之

    神経化学   42 ( 2-3 )   356 - 356   2003.8

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    Language:English   Publisher:(一社)日本神経化学会  

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  • AMPA型グルタミン酸受容体のC末端を介した受容体内在化機構

    岩倉 百合子, 堀川 洋, 茨木 京子, 永野 忠聖, 川村 名子, 武井 延之, 那波 宏之

    神経化学   40 ( 2-3 )   447 - 447   2001.9

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    Language:Japanese   Publisher:(一社)日本神経化学会  

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  • Development of neurites, dendritic filopodia, and synaptic spines in hippocampal low-density culture

    T Nagano, Y Iwakura, T Ushiki, H Nawa

    NEURAL DEVELOPMENT-BOOK   2 ( 2 )   386 - 393   1999

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    Language:English   Publishing type:Article, review, commentary, editorial, etc. (international conference proceedings)  

    Web of Science

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  • Molecular Development of Hippocampal Synapses in Culture

    NAWA Hiroyuki, IWAKURA Yuriko, NAGANO Takashi, USHIKI Tatsuo

    46   A53   1997.12

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Presentations

  • リポポリサッカライドは発達期の大脳皮質神経細胞において上皮成長因子シグナルやシナプス関連分子の発現を撹乱する

    岩倉百合子, 武井延之

    NEURO2024 ( 第47回日本神経科学大会 第67回日本神経化学会大会 第46回日本生物学的精神医学会年会 第8回アジアオセアニア神経科学連合コングレス 合同大会)  2024.7 

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    Presentation type:Poster presentation  

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  • Neurotransmitter-dependent shedding of neureguline-1 precursors in rat forebrain neurons International conference

    Y. Iwakura, R Wang, N Inamura, K Araki, H. Nawa

    第39回日本神経科学大会  2016.7  日本神経科学学会

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    Language:English   Presentation type:Oral presentation (general)  

    Venue:Pacifico Yokohama  

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  • セロトニン神経細胞の発達・成熟に対する選択的な栄養因子シグナルの作用機序の解明

    岩倉百合子, 小林祐太郎, 斎藤摩美, 那波宏之

    第38回日本分子生物学会年会・第88回日本生化学会大会 合同大会  2015.12  日本分子生物学会

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    Language:English   Presentation type:Poster presentation  

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  • 上皮成長因子(EGF)ファミリーと神経伝達物質のクロストーク Invited

    岩倉百合子

    奈良先端未来開拓コロキウム  2014.12  奈良先端大

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    Language:Japanese   Presentation type:Symposium, workshop panel (nominated)  

    Venue:奈良先端大  

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  • Differential neurotrophic signals for serotonergic and dopaminergic development.

    Iwakura Y, Nawa H

    Neuro2013  2013.6  日本神経科学学会、日本神経化学会

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    Language:Japanese   Presentation type:Poster presentation  

    Venue:国立京都国際会館  

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  • Regulated processing / release of neuregulin-1 precursors in rat cortical neurons.

    Iwakura Y, Wang R, Araki K, Nawa H

    第35回日本分子生物学会年会  2012.12  日本分子生物学会

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    Language:English   Presentation type:Symposium, workshop panel (public)  

    Venue:福岡国際会議場  

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  • Regulated processing / release of neuregulin-1 precursors in rat cortical neurons.

    Iwakura Y, Wang R, Araki K, Nawa H

    第34回日本神経科学学会  2011.9  日本神経科学学会

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    Language:English   Presentation type:Poster presentation  

    Venue:パシフィコ横浜  

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  • Dopamine D1 receptor-induced signaling through TrkB receptors in striatal neurons

    Iwakura Y, Nawa H, Sora I, Chao MV

    第51回日本神経化学会  2008.9  日本神経化学会

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    Language:English   Presentation type:Oral presentation (general)  

    Venue:富山国際会議場  

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  • Neurotrophic effects of EGF/ErbB1 signals on developing midbrain dopaminergic neurons.

    Iwakura Y, Zhen Y, Piao YS, Yokomaku D, Aoki H, Takei N, Nawa H

    Neuro2007  2007.9  日本神経科学学会、日本神経化学会

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    Language:English   Presentation type:Oral presentation (general)  

    Venue:パシフィコ横浜  

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Awards

  • 日本神経化学会奨励賞

    2012.9   日本神経化学会  

    岩倉百合子

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    Award type:Honored in official journal of a scientific society, scientific journal  Country:Japan

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Research Projects

  • 血液を用いた脳神経損傷を予測する新規バイオマーカーの研究

    Grant number:25K12292

    2025.4 - 2028.3

    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

    吉田 至誠, 棗田 学, 岡田 正康, 岩倉 百合子, 西山 慶

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    Grant amount:\4680000 ( Direct Cost: \3600000 、 Indirect Cost:\1080000 )

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  • Do antidepressants promote the wound healing of the diabetes?

    Grant number:20K09860

    2020.4 - 2023.3

    System name:Grants-in-Aid for Scientific Research

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

    Awarding organization:Japan Society for the Promotion of Science

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    Grant amount:\4290000 ( Direct Cost: \3300000 、 Indirect Cost:\990000 )

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  • ペリニューロナルネット調節を介したGABA神経への脳内栄養因子の作用機序の解明

    2018.4 - 2021.3

    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

    岩倉百合子, 難波寿明, 武井延之

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    Authorship:Principal investigator  Grant type:Competitive

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  • ペリニューロナルネット調節を介したGABA神経への脳内栄養因子の作用機序の解明

    2017.4

    System name:科学研究費補助金

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    Grant type:Competitive

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  • セロトニン神経路の発達・成熟に対する栄養因子の作用機序の解明

    2013.4 - 2016.3

    System name:科学研究費助成事業

    Research category:若手研究(B)

    Awarding organization:日本学術振興会

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    Grant type:Competitive

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  • ニューレグリンとセロトニン伝達の相互作用

    2012.12

    System name:内藤記念女性研究者研究助成金

    Awarding organization:民間財団等

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    Grant type:Competitive

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  • 神経栄養因子ニューレグリン1の神経伝達物質依存的な切断・放出とその生理的意義

    2012.4 - 2014.3

    System name:科学研究費助成事業

    Research category:若手研究(B)

    Awarding organization:日本学術振興会

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    Grant type:Competitive

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  • ニューレグリンとモノアミン伝達の相互作用

    2011.4 - 2012.3

    System name:上原生命科学財団 研究奨励金

    Awarding organization:民間財団等

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    Grant type:Competitive

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  • モノアミン神経の発達・成熟に対する栄養因子の作用機序の解明

    2010

    System name:科学研究費補助金

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    Grant type:Competitive

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  • 上皮成長因子EGFファミリーと神経伝達物質のクロストーク

    2007.2

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    Grant type:Competitive

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  • ドパミンによる脳由来神経栄養因子(BDNF)受容体(TrkB)のトランスアクティベーション

    2005.4 - 2008

    System name:その他の研究制度

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    Grant type:Competitive

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  • 脳由来神経栄養因子TrkBのドパミンによるトランスアクティベーションメカニズムの解明

    2005.4 - 2007.3

    System name:上原生命科学財団 海外留学助成金

    Awarding organization:民間財団等

    岩倉百合子

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    Authorship:Principal investigator  Grant type:Competitive

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  • 脳内サイトカインによるシナプス発達阻害機構

    2003.4 - 2005.3

    System name:科学研究費助成事業

    Research category:特別研究員推奨費

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    Grant type:Competitive

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  • ドパミン刺激によるEGF/ErbB1シグナルの制御

    2002 - 2005

    System name:科学研究費補助金

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    Grant type:Competitive

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Teaching Experience (researchmap)

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Teaching Experience

  • 薬理学実習

    2018

  • 医学入門

    2017
    -
    2018
    Institution name:新潟大学

  • 生化学実習

    2016
    -
    2023

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    Level:Undergraduate (specialized) 

  • 分子生物学

    2016
    -
    2020
    Institution name:新潟大学

  • 脳と心の医科学

    2016
    -
    2017
    Institution name:新潟大学

  • 先端医科学研究概説

    2012
    -
    2013
    Institution name:新潟大学

  • 医学研究実習

    2010
    -
    2023
    Institution name:新潟大学

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Social Activities

  • スーパーサイエンスハイスクール 実習/研修受け入れ

    Role(s): Lecturer, Demonstrator

    2017.8

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    Audience: High school students

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  • 世界脳週間

    Role(s): Lecturer, Advisor, Organizing member, Demonstrator

    新潟大学脳研究所  2008.3

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    Audience: High school students

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  • スプリングサイエンスキャンプ

    Role(s): Lecturer, Organizing member, Demonstrator

    2008.3 - 2015.3

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    Audience: High school students

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Academic Activities

  • 文部科学省科学技術政策研究所 科学技術動向研究センター 専門調査員

    Role(s): Planning/Implementing academic research

    文部科学省科学技術政策研究所 科学技術動向研究センター  2014

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    Type:Academic research 

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