Updated on 2026/03/07

写真a

 
KAWAMURA Meiko
 
Organization
Academic Assembly Institute of Medicine and Dentistry Specially Appointed Assistant
Graduate School of Medical and Dental Sciences Specially Appointed Assistant
Title
Specially Appointed Assistant
Contact information
メールアドレス
External link

Degree

  • 博士(医学) ( 1995.3   京都大学 )

Research Interests

  • Neurochemistry

  • Virology

  • 感染免疫学

  • molecular biology

Research Areas

  • Life Science / Medical biochemistry

Research History (researchmap)

  • Niigata University, Institute for Research Administration   Center for Coordination of Research Facilities, Division of Instrumental Analysis   Project Assistant Professor

    2023.4

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  • Niigata University   Brain Research Institute Basic Neuroscience Branch   Specially Appointed Assistant Professor

    2015.4 - 2023.3

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  • Niigata Seiryo University

    2001.4

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Research History

  • Niigata University   Graduate School of Medical and Dental Sciences   Specially Appointed Assistant

    2025.4

  • Niigata University   Institute of Medicine and Dentistry, Academic Assembly   Specially Appointed Assistant

    2025.4

  • Niigata University   Center for Coordination of Research Facilities   Specially Appointed Assistant Professor

    2023.4 - 2025.3

  • Niigata University   Brain Research Institute   Specially Appointed Assistant Professor

    2022.8 - 2023.3

  • Niigata University   Brain Research Institute Basic Neuroscience Branch   Specially Appointed Assistant Professor

    2015.4 - 2022.7

Education

  • Hokkaido University   Graduate School, Division of Veterinary Medicine   Department of Epizootiology

    1983.4 - 1985.3

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    Country: Japan

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  • Hokkaido University   Faculty of Veterinary Medicine   Department of Epizootiology

    1979.4 - 1983.3

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    Country: Japan

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Professional Memberships

Qualification acquired

  • Veterinarian

 

Papers

  • 自己免疫性脳炎/自己免疫疾患と精神科臨床 自己免疫性脳炎の広がりと抗体検査を巡る話題

    田中 惠子, 川村 名子, 崎村 建司, 阿部 学

    精神神経学雑誌   ( 2024特別号 )   S647 - S647   2024.6

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

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  • Pathogenesis, Clinical Features, and Treatment of Patients with Myelin Oligodendrocyte Glycoprotein (MOG) Autoantibody-Associated Disorders Focusing on Optic Neuritis with Consideration of Autoantibody-Binding Sites: A Review Reviewed

    Keiko Tanaka, Takeshi Kezuka, Hitoshi Ishikawa, Masami Tanaka, Kenji Sakimura, Manabu Abe, Meiko Kawamura

    International Journal of Molecular Sciences   24 ( 17 )   13368 - 13368   2023.8

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    Publishing type:Research paper (scientific journal)   Publisher:MDPI AG  

    Although there is a substantial amount of data on the clinical characteristics, diagnostic criteria, and pathogenesis of myelin oligodendrocyte glycoprotein (MOG) autoantibody-associated disease (MOGAD), there is still uncertainty regarding the MOG protein function and the pathogenicity of anti-MOG autoantibodies in this disease. It is important to note that the disease characteristics, immunopathology, and treatment response of MOGAD patients differ from those of anti-aquaporin 4 antibody-positive neuromyelitis optica spectrum disorders (NMOSDs) and multiple sclerosis (MS). The clinical phenotypes of MOGAD are varied and can include acute disseminated encephalomyelitis, transverse myelitis, cerebral cortical encephalitis, brainstem or cerebellar symptoms, and optic neuritis. The frequency of optic neuritis suggests that the optic nerve is the most vulnerable lesion in MOGAD. During the acute stage, the optic nerve shows significant swelling with severe visual symptoms, and an MRI of the optic nerve and brain lesion tends to show an edematous appearance. These features can be alleviated with early extensive immune therapy, which may suggest that the initial attack of anti-MOG autoantibodies could target the structures on the blood–brain barrier or vessel membrane before reaching MOG protein on myelin or oligodendrocytes. To understand the pathogenesis of MOGAD, proper animal models are crucial. However, anti-MOG autoantibodies isolated from patients with MOGAD do not recognize mouse MOG efficiently. Several studies have identified two MOG epitopes that exhibit strong affinity with human anti-MOG autoantibodies, particularly those isolated from patients with the optic neuritis phenotype. Nonetheless, the relations between epitopes on MOG protein remain unclear and need to be identified in the future.

    DOI: 10.3390/ijms241713368

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  • Vasopressin Expressed in Hypothalamic CRF Neurons Causes Impaired Water Diuresis in Secondary Adrenal Insufficiency Reviewed

    Satoshi Yamagata, Ashraf H Talukder, Shingo Murasawa, Kanako Niioka, Naoya Kumagai, Mao Takagi, Meiko Kawamura, Rie Natsume, Manabu Abe, Katsuya Uchida, Tatsuya Sato, Akira Kurose, Kazunori Kageyama, Makoto Daimon, Kenji Sakimura, Keiichi Itoi

    Endocrinology   164 ( 8 )   2023.6

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    Publishing type:Research paper (scientific journal)   Publisher:The Endocrine Society  

    Abstract

    Patients with secondary adrenal insufficiency can present with impaired free water excretion and hyponatremia, which is due to the enhanced secretion of vasopressin (AVP) despite increased total body water. AVP is produced in magnocellular neurons in the paraventricular nucleus of the hypothalamus (PVH) and supraoptic nucleus and in parvocellular corticotropin-releasing factor (CRF) neurons in the PVH. This study aimed to elucidate whether magnocellular AVP neurons or parvocellular CRF neurons coexpressing AVP are responsible for the pathogenesis of hyponatremia in secondary adrenal insufficiency. The number of CRF neurons expressing copeptin, an AVP gene product, was significantly higher in adrenalectomized AVP-floxed mice (AVPfl/fl) than in sham-operated controls. Adrenalectomized AVPfl/fl mice supplemented with aldosterone showed impaired water diuresis under ad libitum access to water or after acute water loading. They became hyponatremic after acute water loading, and it was revealed under such conditions that aquaporin-2 (AQP2) protein levels were increased in the kidney. Furthermore, translocation of AQP2 to the apical membrane was markedly enhanced in renal collecting duct epithelial cells. Remarkably, all these abnormalities observed in the mouse model for secondary adrenal insufficiency were ameliorated in CRF-AVP−/− mice that lacked AVP in CRF neurons. Our study demonstrates that CRF neurons in the PVH are responsible for the pathogenesis of impaired water excretion in secondary adrenal insufficiency.

    DOI: 10.1210/endocr/bqad109

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    Other Link: https://academic.oup.com/endo/article-pdf/164/8/bqad109/50976215/bqad109.pdf

  • 自己免疫性疾患/脳炎・脳症と精神症状 認知症および様々な神経変性疾患との鑑別を要する自己免疫性脳炎

    田中 惠子, 川村 名子, 崎村 建司, 阿部 学

    精神神経学雑誌   ( 2023特別号 )   S341 - S341   2023.6

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  • Activity-induced secretion of semaphorin 3A mediates learning. Reviewed International journal

    Aoi Jitsuki-Takahashi, Susumu Jitsuki, Naoya Yamashita, Meiko Kawamura, Manabu Abe, Kenji Sakimura, Akane Sano, Fumio Nakamura, Yoshio Goshima, Takuya Takahashi

    The European journal of neuroscience   53 ( 10 )   3279 - 3293   2021.5

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    The semaphorin family is a well-characterized family of secreted or membrane-bound proteins that are involved in activity-independent neurodevelopmental processes, such as axon guidance, cell migration, and immune functions. Although semaphorins have recently been demonstrated to regulate activity-dependent synaptic scaling, their roles in Hebbian synaptic plasticity as well as learning and memory remain poorly understood. Here, using a rodent model, we found that an inhibitory avoidance task, a hippocampus-dependent contextual learning paradigm, increased secretion of semaphorin 3A in the hippocampus. Furthermore, the secreted semaphorin 3A in the hippocampus mediated contextual memory formation likely by driving AMPA receptors into hippocampal synapses via the neuropilin1-plexin A4-semaphorin receptor complex. This signaling process involves alteration of the phosphorylation status of collapsin response mediator protein 2, which has been characterized as a downstream molecule in semaphorin signaling. These findings implicate semaphorin family as a regulator of Hebbian synaptic plasticity and learning.

    DOI: 10.1111/ejn.15210

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  • Central dopamine D2 receptors regulate plasma glucose levels in mice through autonomic nerves Reviewed

    Hiroko Ikeda, Naomi Yonemochi, Risa Mikami, Manabu Abe, Meiko Kawamura, Rie Natsume, Kenji Sakimura, John L. Waddington, Junzo Kamei

    Scientific Reports   10 ( 1 )   2020.12

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

    <title>Abstract</title>Recent evidence suggests that the central nervous system (CNS) regulates plasma glucose levels, but the underlying mechanism is unclear. The present study investigated the role of dopaminergic function in the CNS in regulation of plasma glucose levels in mice. I.c.v. injection of neither the dopamine D<sub>1</sub> receptor agonist SKF 38393 nor the antagonist SCH 23390 influenced plasma glucose levels. In contrast, i.c.v. injection of both the dopamine D<sub>2</sub> receptor agonist quinpirole and the antagonist l-sulpiride increased plasma glucose levels. Hyperglycemia induced by quinpirole and l-sulpiride was absent in dopamine D<sub>2</sub> receptor knockout mice. I.c.v. injection of quinpirole and l-sulpiride each increased mRNA levels of hepatic glucose-6-phosphatase and phosphoenolpyruvate carboxykinase, which are the key enzymes for hepatic gluconeogenesis. Systemic injection of the β<sub>2</sub> adrenoceptor antagonist ICI 118,551 inhibited hyperglycemia induced by l-sulpiride, but not by quinpirole. In contrast, hyperglycemia induced by quinpirole, but not by l-sulpiride, was inhibited by hepatic vagotomy. These results suggest that stimulation of central dopamine D<sub>2</sub> receptors increases plasma glucose level by increasing hepatic glucose production through parasympathetic nerves, whereas inhibition of central dopamine D<sub>2</sub> receptors increases plasma glucose level by increasing hepatic glucose production through sympathetic nerves.

    DOI: 10.1038/s41598-020-79292-0

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    Other Link: http://www.nature.com/articles/s41598-020-79292-0

  • Significance of Autoantibodies in Autoimmune Encephalitis in Relation to Antigen Localization: An Outline of Frequently Reported Autoantibodies with a Non-Systematic Review. Reviewed International journal

    Keiko Tanaka, Meiko Kawamura, Kenji Sakimura, Nobuo Kato

    International journal of molecular sciences   21 ( 14 )   2020.7

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    Autoantibodies related to central nervous system (CNS) diseases propel research on paraneoplastic neurological syndrome (PNS). This syndrome develops autoantibodies in combination with certain neurological syndromes and cancers, such as anti-HuD antibodies in encephalomyelitis with small cell lung cancer and anti-Yo antibodies in cerebellar degeneration with gynecological cancer. These autoantibodies have roles in the diagnosis of neurological diseases and early detection of cancers that are usually occult. Most of these autoantibodies have no pathogenic roles in neuronal dysfunction directly. Instead, antigen-specific cytotoxic T lymphocytes are thought to have direct roles in neuronal damage. The recent discoveries of autoantibodies against neuronal synaptic receptors/channels produced in patients with autoimmune encephalomyelitis have highlighted insights into our understanding of the variable neurological symptoms in this disease. It has also improved our understanding of intractable epilepsy, atypical psychosis, and some demyelinating diseases that are ameliorated with immune therapies. The production and motility of these antibodies through the blood-brain barrier into the CNS remains unknown. Most of these recently identified autoantibodies bind to neuronal and glial cell surface synaptic receptors, potentially altering the synaptic signaling process. The clinical features differ among pathologies based on antibody targets. The investigation of these antibodies provides a deeper understanding of the background of neurological symptoms in addition to novel insights into their basic neuroscience.

    DOI: 10.3390/ijms21144941

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  • Expression mapping, quantification, and complex formation of GluD1 and GluD2 glutamate receptors in adult mouse brain. Reviewed International journal

    Chihiro Nakamoto, Kohtarou Konno, Taisuke Miyazaki, Ena Nakatsukasa, Rie Natsume, Manabu Abe, Meiko Kawamura, Yugo Fukazawa, Ryuichi Shigemoto, Miwako Yamasaki, Kenji Sakimura, Masahiko Watanabe

    The Journal of comparative neurology   528 ( 6 )   1003 - 1027   2020.4

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    In the cerebellum, GluD2 is exclusively expressed in Purkinje cells, where it regulates synapse formation and regeneration, synaptic plasticity, and motor learning. Delayed cognitive development in humans with GluD2 gene mutations suggests extracerebellar functions of GluD2. However, extracerebellar expression of GluD2 and its relationship with that of GluD1 are poorly understood. GluD2 mRNA and protein were widely detected, with relatively high levels observed in the olfactory glomerular layer, medial prefrontal cortex, cingulate cortex, retrosplenial granular cortex, olfactory tubercle, subiculum, striatum, lateral septum, anterodorsal thalamic nucleus, and arcuate hypothalamic nucleus. These regions were also enriched for GluD1, and many individual neurons coexpressed the two GluDs. In the retrosplenial granular cortex, GluD1 and GluD2 were selectively expressed at PSD-95-expressing glutamatergic synapses, and their coexpression on the same synapses was shown by SDS-digested freeze-fracture replica labeling. Biochemically, GluD1 and GluD2 formed coimmunoprecipitable complex formation in HEK293T cells and in the cerebral cortex and hippocampus. We further estimated the relative protein amount by quantitative immunoblotting using GluA2/GluD2 and GluA2/GluD1 chimeric proteins as standards for titration of GluD1 and GluD2 antibodies. Intriguingly, the relative amount of GluD2 was almost comparable to that of GluD1 in the postsynaptic density fraction prepared from the cerebral cortex and hippocampus. In contrast, GluD2 was overwhelmingly predominant in the cerebellum. Thus, we have determined the relative extracerebellar expression of GluD1 and GluD2 at regional, neuronal, and synaptic levels. These data provide a molecular-anatomical basis for possible competitive and cooperative interactions of GluD family members at synapses in various brain regions.

    DOI: 10.1002/cne.24792

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  • GluD1 knockout mice with a pure C57BL/6N background show impaired fear memory, social interaction, and enhanced depressive-like behavior. Reviewed International journal

    Chihiro Nakamoto, Meiko Kawamura, Ena Nakatsukasa, Rie Natsume, Keizo Takao, Masahiko Watanabe, Manabu Abe, Tomonori Takeuchi, Kenji Sakimura

    PloS one   15 ( 2 )   e0229288   2020

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    The GluD1 gene is associated with susceptibility for schizophrenia, autism, depression, and bipolar disorder. However, the function of GluD1 and how it is involved in these conditions remain elusive. In this study, we generated a Grid1 gene-knockout (GluD1-KO) mouse line with a pure C57BL/6N genetic background and performed several behavioral analyses. Compared to a control group, GluD1-KO mice showed no significant anxiety-related behavioral differences, evaluated using behavior in an open field, elevated plus maze, a light-dark transition test, the resident-intruder test of aggression and sensorimotor gating evaluated by the prepulse inhibition test. However, GluD1-KO mice showed (1) higher locomotor activity in the open field, (2) decreased sociability and social novelty preference in the three-chambered social interaction test, (3) impaired memory in contextual, but not cued fear conditioning tests, and (4) enhanced depressive-like behavior in a forced swim test. Pharmacological studies revealed that enhanced depressive-like behavior in GluD1-KO mice was restored by the serotonin reuptake inhibitors imipramine and fluoxetine, but not the norepinephrine transporter inhibitor desipramine. In addition, biochemical analysis revealed no significant difference in protein expression levels, such as other glutamate receptors in the synaptosome and postsynaptic densities prepared from the frontal cortex and the hippocampus. These results suggest that GluD1 plays critical roles in fear memory, sociability, and depressive-like behavior.

    DOI: 10.1371/journal.pone.0229288

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  • Dissociating orexin-dependent and -independent functions of orexin neurons using novel Orexin-Flp knock-in mice. Reviewed International journal

    Srikanta Chowdhury, Chi Jung Hung, Shuntaro Izawa, Ayumu Inutsuka, Meiko Kawamura, Takashi Kawashima, Haruhiko Bito, Itaru Imayoshi, Manabu Abe, Kenji Sakimura, Akihiro Yamanaka

    eLife   8   2019.6

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    Uninterrupted arousal is important for survival during threatening situations. Activation of orexin/hypocretin neurons is implicated in sustained arousal. However, orexin neurons produce and release orexin as well as several co-transmitters including dynorphin and glutamate. To disambiguate orexin-dependent and -independent physiological functions of orexin neurons, we generated a novel Orexin-flippase (Flp) knock-in mouse line. Crossing with Flp-reporter or Cre-expressing mice showed gene expression exclusively in orexin neurons. Histological studies confirmed that orexin was knock-out in homozygous mice. Orexin neurons without orexin showed altered electrophysiological properties, as well as received decreased glutamatergic inputs. Selective chemogenetic activation revealed that both orexin and co-transmitters functioned to increase wakefulness, however, orexin was indispensable to promote sustained arousal. Surprisingly, such activation increased the total time spent in cataplexy. Taken together, orexin is essential to maintain basic membrane properties and input-output computation of orexin neurons, as well as to exert awake-sustaining aptitude of orexin neurons.

    DOI: 10.7554/eLife.44927

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  • Autophosphorylation of F-actin binding domain of CaMKIIβ is required for fear learning. Reviewed International journal

    Karam Kim, Akio Suzuki, Hiroto Kojima, Meiko Kawamura, Ken Miya, Manabu Abe, Ikuko Yamada, Tamio Furuse, Shigenaru Wakana, Kenji Sakimura, Yasunori Hayashi

    Neurobiology of learning and memory   157   86 - 95   2019.1

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    CaMKII is a pivotal kinase that plays essential roles in synaptic plasticity. Apart from its signaling function, the structural function of CaMKII is becoming clear. CaMKII - F-actin interaction stabilizes actin cytoskeleton in a dendritic spine. A transient autophosphorylation at the F-actin binding region during LTP releases CaMKII from F-actin and opens a brief time-window of actin reorganization. However, the physiological relevance of this finding in learning and memory was not presented. Using a knock-in (KI) mouse carrying phosphoblock mutations in the actin-binding domain of CaMKIIβ, we demonstrate that proper regulation of CaMKII - F-actin interaction is important for fear conditioning memory tasks. The KI mice show poor performance in contextual and cued versions of fear conditioning test. These results suggest the importance of CaMKII - F-actin interactions in learning and memory.

    DOI: 10.1016/j.nlm.2018.12.003

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  • Higher visual responses in the temporal cortex of mice Reviewed

    Nishino K, Tsukano H, Hishida R, Abe M, Nakai J, Kawamura M, Aiba A, Sakimura K, Shibuki K

    Scientific reports   2018

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  • GLUD1 deficient mouse as a model animal of depressionlike behavior

    K. Sakimura, C. Nakamoto, M. Abe, M. Kawamura, H. Uchida, M. Watanabe, M. Kano

    JOURNAL OF NEUROCHEMISTRY   142   203 - 203   2017.8

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  • Retrograde BDNF to TrkB signaling promotes synapse elimination in the developing cerebellum Reviewed

    Myeongjeong Choo, Taisuke Miyazaki, Maya Yamazaki, Meiko Kawamura, Takanobu Nakazawa, Jianling Zhang, Asami Tanimura, Naofumi Uesaka, Masahiko Watanabe, Kenji Sakimura, Masanobu Kano

    NATURE COMMUNICATIONS   8 ( 195 )   2017.8

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    DOI: 10.1038/s41467-017-00260-w

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  • The cellular and behavioral consequences of interleukin-1 alpha penetration through the blood-brain barrier of neonatal rats: A critical period for efficacy Reviewed

    M. Tohmi, N. Tsuda, Y. Zheng, M. Mizuno, H. Sotoyama, M. Shibuya, M. Kawamura, A. Kakita, H. Takahashi, H. Nawa

    NEUROSCIENCE   150 ( 1 )   234 - 250   2007.11

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    DOI: 10.1016/j.neuroscience.2007.08.034

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  • Association of 14-3-3 epsilon gene haplotype with completed suicide in Japanese Reviewed

    M Yanagi, O Shirakawa, N Kitamura, K Okamura, K Sakurai, N Nishiguchi, T Hashimoto, H Nushida, Y Ueno, D Kanbe, M Kawamura, K Araki, H Nawa, K Maeda

    JOURNAL OF HUMAN GENETICS   50 ( 4 )   210 - 216   2005.4

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    DOI: 10.1007/s10038-005-0241-0

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  • Brain-derived neurotrophic factor induces mammalian target of rapamycin-dependent local activation of translation machinery and protein synthesis in neuronal dendrites Reviewed

    Takei N, Inamura N, Kawamura M, Namba H, Hara K, Yonezawa K, Nawa H

    JOURNAL OF NEUROSCIENCE   24 ( 44 )   9760 - 9769   2004.11

  • Prefrontal abnormality of schizophrenia revealed by DNA microarray: Impact on glial and neurotrophic gene expression Reviewed

    Tetsuji Sugai, Meiko Kawamura, Shuji Iritani, Kazuaki Araki, Takao Makifuchi, China Imai, Ryosuke Nakamura, Akiyoshi Kakita, Hitoshi Takahashi, Hiroyuki Nawa

    Annals of the New York Academy of Sciences   1025   84 - 91   2004

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    DOI: 10.1196/annals.1316.011

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  • Prefrontal abnormality of schizophrenia revealed by DNA microarray - Impact on glial and neurotrophic gene expression Reviewed

    Sugai T, Kawamura M, Iritani S, Araki K, Makifuchi T, Imai C, Nakamura R, Kakita A, Takahashi H, Nawa H

    CURRENT STATUS OF DRUG DEPENDENCE / ABUSE STUDIES: CELLULAR AND MOLECULAR MECHANISMS OF DRUGS OF ABUSE AND NEUROTOXICITY   1025   84 - 91   2004

  • A palmitoylated RING finger ubiquitin ligase and its homologue in the brain membranes Reviewed

    K Araki, M Kawamura, T Suzuki, N Matsuda, D Kanbe, K Ishii, T Ichikawa, T Kumanishi, T Chiba, K Tanaka, H Nawa

    JOURNAL OF NEUROCHEMISTRY   86 ( 3 )   749 - 762   2003.8

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    DOI: 10.1046/j.1471-4159.2003.01875.x

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  • Characterization of novel bicistronic Sindbis virus vectors, SinEGdsp and SinIRES-EG, in cultured neurons. (Minireview)

    Kawamura M, Namba H, Otsu Y, Hayashi Y, Takei N. Nawa H

    Recent Research Development in Neurochemistry   2003

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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

    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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  • Brain-derived neurotrophic factor enhances neuronal translation by activating multiple initiation processes: comparison with the effects of insulin. Reviewed

    Takei N, Kawamura M, Hara K, Yonezawa K, Nawa H

    J Biol Chem.   276 ( 46 )   42818 - 42825   2001.12

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    DOI: 10.1074/jbc.M103237200

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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 decoys Reviewed

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

    JOURNAL OF BIOLOGICAL CHEMISTRY   276 ( 43 )   40025 - 40032   2001.10

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    DOI: 10.1074/jbc.M103125200

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  • Sindbis viral-mediated expression of Ca2+-permeable AMPA receptors at hippocampal CA1 synapses and induction of NMDA receptor-independent long-term potentiation Reviewed

    T Okada, N Yamada, W Kakegawa, K Tsuzuki, M Kawamura, H Nawa, M Iino, S Ozawa

    EUROPEAN JOURNAL OF NEUROSCIENCE   13 ( 8 )   1635 - 1643   2001.4

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    DOI: 10.1046/j.0953-816x.2001.01523.x

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  • Regulation of nerve growth factor release by nitric oxide through cyclic GMP pathway in cortical glial cells Reviewed

    HB Xiong, K Yamada, H Jourdi, M Kawamura, N Takei, DK Han, T Nabeshima, H Nawa

    MOLECULAR PHARMACOLOGY   56 ( 2 )   339 - 347   1999.8

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  • Cell-dependent replication potentials of HIV-1 gag mutants. Reviewed

    Adachi, A, Tamaki, M, Shimano, R, Inubushi, R, Naito, T, Yoshida, K, Oshima, Y, Kawamura, M, Koyama, A.H

    Microbes and Infection   1 ( 9 )   671 - 676   1999

  • Enhancement of human immunodeficiency virus type 1 infectivity by Nef is producer cell-dependent Reviewed

    K Tokunaga, A Kojima, T Kurata, K Ikuta, H Akari, AH Koyama, M Kawamura, R Inubushi, R Shimano, A Adachi

    JOURNAL OF GENERAL VIROLOGY   79   2447 - 2453   1998.10

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  • Suppression of HIV replication by dominant negative mutants of HIV-1 (Review) Reviewed

    R Inubushi, R Shimano, Y Oshima, K Yoshida, M Kawamura, A Adachi

    INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE   2 ( 3 )   325 - 330   1998.9

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  • Early function of HIV-1 Gag proteins is cell-dependent Reviewed

    M Kawamura, R Shimano, R Inubushi, H Akari, A Adachi

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS   248 ( 3 )   899 - 903   1998.7

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    DOI: 10.1006/bbrc.1998.9065

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  • Suppression of HIV-2 replication by HIV-1 gag mutants Reviewed

    R Shimano, R Inubushi, T Fukumori, M Tamaki, Y Oshima, M Kawamura, A Adachi

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS   248 ( 2 )   418 - 421   1998.7

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    DOI: 10.1006/bbrc.1998.8975

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  • Inhibition of HIV replication by capsid mutant C6b Reviewed

    R Shimano, S Iida, T Fukumori, Y Yamamoto, M Kawamura, RA Furuta, A Adachi

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS   242 ( 2 )   313 - 316   1998.1

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    DOI: 10.1006/bbrc.1997.7963

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  • Complete inhibition of SIVmac replication by its capsid mutants Reviewed

    R Shimano, R Inubushi, K Amano, T Ogasawara, H Akari, AH Koyama, M Kawamura, A Adachi

    VIRUS GENES   17 ( 1 )   43 - 48   1998

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    DOI: 10.1023/A:1008001000878

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  • Mapping the genetic determinants of human immunodeficiency virus type 2 for cell tropism and replication efficiency Reviewed

    M Kawamura, R Shimano, T Ogasawara, R Inubushi, K Amano, H Akari, A Adachi

    ARCHIVES OF VIROLOGY   143 ( 3 )   513 - 521   1998

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  • Producer cell-dependent requirement of the Nef protein for efficient entry of HIV-1 into cells. Reviewed

    Tokunaga, K, Kojima, A, Kurata, T, Ikuta, K, Inubushi, R, Shimano, R, Kawamura, M, Akari, H, Koyama, A.H, Adachi, A

    Biochemical and Biophysical Research Communications   250 ( 3 )   565 - 568   1998

  • Functional domain mapping of HIV-1 gag proteins Reviewed

    M Kawamura, R Shimano, R Inubushi, K Amano, T Ogasawara, H Akari, A Adachi

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS   241 ( 2 )   317 - 320   1997.12

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  • Cleavage of Gag precursor is required for early replication phase of HIV-1 Reviewed

    M Kawamura, R Shimano, R Inubushi, K Amano, T Ogasawara, H Akari, A Adachi

    FEBS LETTERS   415 ( 2 )   227 - 230   1997.9

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  • HIV-1 capsid mutants inhibit the replication of wild-type virus at both early and late infection phases Reviewed

    RA Furuta, R Shimano, T Ogasawara, R Inubushi, K Amano, H Akari, M Hatanaka, M Kawamura, A Adachi

    FEBS LETTERS   415 ( 2 )   231 - 234   1997.9

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  • Methods for HIV/SIV gene analysis Invited Reviewed

    Adachi A, Kawamura M, Tokunaga K, Sakai H

    Viral Genome Mothods, chapter 3   3   43 - 53   1996

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  • EARLY REPLICATION BLOCK OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 IN MONKEY CELLS Reviewed

    R SHIBATA, H SAKAI, M KAWAMURA, K TOKUNAGA, A ADACHI

    JOURNAL OF GENERAL VIROLOGY   76   2723 - 2730   1995.11

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  • FUNCTION OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 VPU PROTEIN IN VARIOUS CELL-TYPES Reviewed

    H SAKAI, K TOKUNAGA, M KAWAMURA, A ADACHI

    JOURNAL OF GENERAL VIROLOGY   76   2717 - 2722   1995.11

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  • GENERATION AND CHARACTERIZATION OF A HOST CELL-DEPENDENT GAG GENE MUTANT OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 Reviewed

    J SAKURAGI, H SAKAI, M KAWAMURA, K TOKUNAGA, S UEDA, A ADACHI

    VIROLOGY   212 ( 1 )   251 - 254   1995.9

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  • REV-DEPENDENCY OF EXPRESSION OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 GAG AND ENV GENES Reviewed

    H SAKAI, RA FURUTA, K TOKUNAGA, M KAWAMURA, M HATANAKA, A ADACHI

    FEBS LETTERS   365 ( 2-3 )   141 - 145   1995.5

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  • Functionality of chimeric Rev proteins of HIV SIV Reviewed

    RA Furuta, H Sakai, M Kawamura, K Tokunaga, M Hatanaka, A Adachi

    VIRUS GENES   11 ( 1 )   11 - 14   1995

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  • Functional analysis of human spuma retrovirus genome Reviewed

    A Adachi, H Sakai, K Tokunaga, M Kawamura

    VIRUS GENES   11 ( 1 )   15 - 20   1995

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  • GROWTH ABILITY OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 AUXILIARY GENE MUTANTS IN PRIMARY BLOOD MACROPHAGE CULTURES Reviewed

    M KAWAMURA, T ISHIZAKI, A ISHIMOTO, T SHIODA, T KITAMURA, A ADACHI

    JOURNAL OF GENERAL VIROLOGY   75   2427 - 2431   1994.9

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  • HUMAN-IMMUNODEFICIENCY-VIRUS VPX IS REQUIRED FOR THE EARLY PHASE OF REPLICATION IN PERIPHERAL-BLOOD MONONUCLEAR-CELLS Reviewed

    M KAWAMURA, H SAKAI, A ADACHI

    MICROBIOLOGY AND IMMUNOLOGY   38 ( 11 )   871 - 878   1994

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  • CELL-DEPENDENT REQUIREMENT OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 VIF PROTEIN FOR MATURATION OF VIRUS-PARTICLES Reviewed

    H SAKAI, R SHIBATA, J SAKURAGI, S SAKURAGI, M KAWAMURA, A ADACHI

    JOURNAL OF VIROLOGY   67 ( 3 )   1663 - 1666   1993.3

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  • INTEGRATION IS ESSENTIAL FOR EFFICIENT GENE-EXPRESSION OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 Reviewed

    H SAKAI, M KAWAMURA, JI SAKURAGI, S SAKURAGI, R SHIBATA, A ISHIMOTO, N ONO, S UEDA, A ADACHI

    JOURNAL OF VIROLOGY   67 ( 3 )   1169 - 1174   1993.3

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  • COMPATIBILITY OF TAT AND REV TRANSACTIVATORS IN THE PRIMATE LENTIVIRUSES Reviewed

    H SAKAI, JI SAKURAGI, S SAKURAGI, M KAWAMURA, A ADACHI

    ARCHIVES OF VIROLOGY   129 ( 1-4 )   1 - 10   1993

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  • ISOLATION AND CHARACTERIZATION OF SIMIAN IMMUNODEFICIENCY VIRUS FROM AFRICAN WHITE-CROWNED MANGABEY MONKEYS (CERCOCEBUS-TORQUATUS-LUNULATUS) Reviewed

    K TOMONAGA, J KATAHIRA, M FUKASAWA, MA HASSAN, M KAWAMURA, H AKARI, T MIURA, T GOTO, M NAKAI, M SULEMAN, M ISAHAKIA, M HAYAMI

    ARCHIVES OF VIROLOGY   129 ( 1-4 )   77 - 92   1993

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  • Structure and function of HIV genes

    M. Kawamura, H. Sakai, A. Adachi

    Nippon rinsho. Japanese journal of clinical medicine   51   31 - 36   1993

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  • INFECTION OF MACAQUE MONKEYS WITH A CHIMERIC HUMAN AND SIMIAN IMMUNODEFICIENCY VIRUS Reviewed

    S SAKURAGI, R SHIBATA, R MUKAI, T KOMATSU, M FUKASAWA, H SAKAI, JI SAKURAGI, M KAWAMURA, K IBUKI, M HAYAMI, A ADACHI

    JOURNAL OF GENERAL VIROLOGY   73   2983 - 2987   1992.11

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  • SEQUENCES RESPONSIBLE FOR EFFICIENT REPLICATION OF SIMIAN IMMUNODEFICIENCY VIRUS SIV(MND) IN CELLS OF THE MONOCYTE MACROPHAGE LINEAGE Reviewed

    H SAKAI, S SAKURAGI, JI SAKURAGI, M KAWAMURA, R SHIBATA, A ADACHI

    JOURNAL OF GENERAL VIROLOGY   73   2989 - 2993   1992.11

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  • ISOLATION AND CHARACTERIZATION OF A HIGHLY DIVERGENT HIV-2[GH-2] - GENERATION OF AN INFECTIOUS MOLECULAR CLONE AND FUNCTIONAL-ANALYSIS OF ITS REV-RESPONSIVE ELEMENT IN RESPONSE TO PRIMATE RETROVIRUS TRANSACTIVATORS (REV AND REX) Reviewed

    M KAWAMURA, J KATAHIRA, M FUKASAWA, JI SAKURAGI, KI ISHIKAWA, M NAKAI, JAA MINGLE, M OSEIKWASI, VBA NETTY, H AKARI, O HISHIDA, K TOMONAGA, T MIURA, M HAYAMI

    VIROLOGY   188 ( 2 )   850 - 853   1992.6

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    DOI: 10.1016/0042-6822(92)90540-6

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  • BIOLOGICAL CHARACTERIZATION OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 AND TYPE-2 MUTANTS IN HUMAN PERIPHERAL-BLOOD MONONUCLEAR-CELLS Reviewed

    H AKARI, J SAKURAGI, Y TAKEBE, K TOMONAGA, M KAWAMURA, M FUKASAWA, T MIURA, T SHINJO, M HAYAMI

    ARCHIVES OF VIROLOGY   123 ( 1-2 )   157 - 167   1992

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  • PRODUCTION AND CHARACTERIZATION OF MOUSE MONOCLONAL-ANTIBODIES AGAINST THE TRANSMEMBRANE PROTEIN OF A HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-2 Reviewed

    H KOMATSU, A YAMASHITA, H TOZAWA, Y MIZUTANI, M HONDA, M KAWAMURA, M HAYAMI

    AIDS RESEARCH AND HUMAN RETROVIRUSES   7 ( 12 )   999 - 1005   1991.12

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  • FUNCTIONAL-ANALYSIS OF LONG TERMINAL REPEATS DERIVED FROM 4 STRAINS OF SIMIAN IMMUNODEFICIENCY VIRUS SIVAGM IN RELATION TO OTHER PRIMATE LENTIVIRUSES Reviewed

    J SAKURAGI, M FUKASAWA, R SHIBATA, H SAKAI, M KAWAMURA, H AKARI, T KIYOMASU, A ISHIMOTO, M HAYAMI, A ADACHI

    VIROLOGY   185 ( 1 )   455 - 459   1991.11

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  • COMPATIBILITY OF REV GENE ACTIVITY IN THE 4 GROUPS OF PRIMATE LENTIVIRUSES Reviewed

    H SAKAI, R SHIBATA, J SAKURAGI, T KIYOMASU, M KAWAMURA, M HAYAMI, A ISHIMOTO, A ADACHI

    VIROLOGY   184 ( 2 )   513 - 520   1991.10

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    DOI: 10.1016/0042-6822(91)90421-7

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  • GENERATION OF A CHIMERIC HUMAN AND SIMIAN IMMUNODEFICIENCY VIRUS INFECTIOUS TO MONKEY PERIPHERAL-BLOOD MONONUCLEAR-CELLS Reviewed

    R SHIBATA, M KAWAMURA, H SAKAI, M HAYAMI, A ISHIMOTO, A ADACHI

    JOURNAL OF VIROLOGY   65 ( 7 )   3514 - 3520   1991.7

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  • GEOGRAPHICAL-DISTRIBUTION OF SUBJECTS SEROPOSITIVE FOR HUMAN T-CELL LEUKEMIA-VIRUS TYPE-1 IN PAPUA-NEW-GUINEA Reviewed

    J IMAI, S TERASHI, T TALONU, H KOMODA, T TAUFA, GT NURSE, D BABONA, K YAMAGUCHI, H NAKASHIMA, K ISHIKAWA, M KAWAMURA, M HAYAMI

    JAPANESE JOURNAL OF CANCER RESEARCH   81 ( 12 )   1218 - 1221   1990.12

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  • ESTABLISHMENT OF A PHYLOGENETIC SURVEY SYSTEM FOR AIDS-RELATED LENTIVIRUSES AND DEMONSTRATION OF A NEW HIV-2 SUBGROUP Reviewed

    T MIURA, J SAKURAGI, M KAWAMURA, M FUKASAWA, EN MORIYAMA, T GOJOBORI, K ISHIKAWA, JAA MINGLE, VBA NETTEY, H AKARI, M ENAMI, H TSUJIMOTO, M HAYAMI

    AIDS   4 ( 12 )   1257 - 1261   1990.12

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  • MULTIPLE ANTIGENIC EPITOPES EXPRESSED ON GAG PROTEINS, P26 AND P15, OF A HUMAN-IMMUNODEFICIENCY-VIRUS (HIV) TYPE-2 AS DEFINED WITH A LIBRARY OF MONOCLONAL-ANTIBODIES Reviewed

    H KOMATSU, H TOZAWA, M KAWAMURA, T KODAMA, M HAYAMI

    AIDS RESEARCH AND HUMAN RETROVIRUSES   6 ( 7 )   871 - 881   1990.7

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  • IMMUNOLOGICAL REACTIVITIES OF GHANAIAN SERA WITH HIV-1, HIV-2, AND SIMIAN IMMUNODEFICIENCY VIRUS SIVAGM Reviewed

    M KAWAMURA, K ISHIKAWA, JAA MINGLE, M OSEIKWASI, SN AFOAKWA, VBA NETTEY, TR CHOSA, M HAYAMI

    AIDS   3 ( 9 )   609 - 611   1989.9

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  • HIV-2 IN WEST-AFRICA IN 1966 Reviewed

    MOHAMMED, I, TO HARRY, A NASIDI

    LANCET   1 ( 8647 )   1137 - 1137   1989.5

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  • HIV-2 in west Africa in 1966. Reviewed International journal

    M Kawamura, S Yamazaki, K Ishikawa, T B Kwofie, H Tsujimoto, M Hayami

    Lancet (London, England)   1 ( 8634 )   385 - 385   1989.2

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  • ISOLATION AND CHARACTERIZATION OF HIV-2 FROM AN AIDS PATIENT IN GHANA Reviewed

    K ISHIKAWA, H TSUJIMOTO, M NAKAI, JAA MINGLE, M OSEIKWASI, SE AGGREY, VBA NETTEY, SN AFOAKWA, M FUKASAWA, T KODAMA, M KAWAMURA, M HAYAMI

    AIDS   2 ( 5 )   383 - 388   1988.10

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  • SEROLOGICAL AND PATHOLOGICAL-STUDIES OF NEWCASTLE-DISEASE VIRUSES ISOLATED FROM CAGED BIRDS FROM SOUTHEAST-ASIA Reviewed

    M KAWAMURA, K NEROME, H KODAMA, H IZAWA, T MIKAMI

    AVIAN DISEASES   31 ( 3 )   564 - 569   1987.7

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  • ISOLATION OF ORTHOMYXOVIRUS AND PARAMYXOVIRUS FROM MIGRATING FERAL DUCKS IN JAPAN Reviewed

    T MIKAMI, M KAWAMURA, T KONDO, T MURAI, M HORIUCHI, H KODAMA, H IZAWA, H KIDA

    VETERINARY RECORD   120 ( 17 )   417 - 418   1987.4

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  • ANTIGENIC VARIATION OF NEWCASTLE-DISEASE VIRUSES ISOLATED FROM WILD DUCKS IN JAPAN Reviewed

    M KAWAMURA, K NAGATAMATSUBARA, K NEROME, N YAMANE, H KIDA, H KODAMA, H IZAWA, T MIKAMI

    MICROBIOLOGY AND IMMUNOLOGY   31 ( 8 )   831 - 835   1987

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    DOI: 10.1111/j.1348-0421.1987.tb03144.x

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  • PATHOGENICITY AND IMMUNOGENICITY IN CHICKENS OF NEWCASTLE-DISEASE VIRUSES ISOLATED FROM WILD DUCKS Reviewed

    M KAWAMURA, T MIKAMI, H KODAMA, H IZAWA

    ARCHIVES OF VIROLOGY   95 ( 1-2 )   149 - 156   1987

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  • PATHOGENICITY AND IMMUNOGENICITY IN CHICKENS OF NEWCASTLE-DISEASE VIRUSES ISOLATED FROM WILD DUCKS Reviewed

    M KAWAMURA, T MIKAMI, H KODAMA, H IZAWA

    ARCHIVES OF VIROLOGY   95 ( 1-2 )   149 - 156   1987

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    田中惠子, 田中惠子, 川村名子, 崎村建司, 阿部学

    日本精神神経学会総会プログラム・抄録集   119th   2023

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    田中 惠子, 渡邊 ユリ, 阿部 学, 崎村 建司, 川村 名子

    精神神経学雑誌   124 ( 4付録 )   S - 447   2022.4

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    精神神経学雑誌   ( 2021特別号 )   S294 - S294   2021.9

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  • 生殖巣特異的GATA4欠損マウスの作製とその胚盤胞補完法受容胚としての適性検索

    岩崎亜美, 村田康輔, 川村名子, 中務胞, 阿部学, 夏目里恵, 杉村智史, 崎村建司, 山城秀昭

    日本繁殖生物学会講演要旨集(Web)   114th   2021

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    田中 惠子, 北川 陽子, 堀 喜代江, 渡邉 ユリ, 崎村 建司, 川村 名子

    神経免疫学   25 ( 1 )   160 - 160   2020.10

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  • Generation of GATA4-flox mouse by gene targeting method

    IWASAKI Tsugumi, MURATA Kousuke, KAWAMURA Meiko, NAKATSUKASA Ena, ABE Manabu, NATSUME Rie, SUGIMURA Satoshi, SAKIMURA Kenji, YAMASHIRO Hideaki

    The Journal of Reproduction and Development Supplement   113 ( 0 )   P - 11-P-11   2020

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    DOI: 10.14882/jrds.113.0_P-11

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  • D1/D2ドーパミン受容体コンディショナル発現マウスによる運動制御機構の解明

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    生命科学系学会合同年次大会   2017年度   [4LT08 - 1195)]   2017.12

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  • 脳に高発現する膜結合型,新規ユビキチン・ライゲース(Momo及びSakura)の生化学的解析(Ubiquitin ligase activity and palmitoylation of the membrane-associating RING finger proteins, Momo and Sakura)

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    神経化学   42 ( 2-3 )   270 - 270   2003.8

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

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  • Enhancement of human immunodeficiency virus type 1 infectivity by Nef is producer cell-dependent.

    Tokunaga Kenzo, Kojima Asato, Kurata Takeshi, Ikuta Kazuyoshi, Akari Hirofumi, Koyama Hajime, Kawamura Meiko, Inubushi Ritsuko, Shimano Reika, Adachi Akio

    Collected papers from the Institute of Immunological Science Hokkaido University   21   120 - 126   1998

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  • Producer cell-dependent requirement of the Nef protein for efficient entry of HIV-1 into cells.

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    Collected papers from the Institute of Immunological Science Hokkaido University   21   109 - 112   1998

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  • HIV複製の分子基盤.

    足立昭夫, 川村名子

    医学のあゆみ   176 ( 1 )   17 - 23   1996

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    Other Link: http://search.jamas.or.jp/link/ui/1996061864

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    川村名子, 徳永研三, 足立昭夫

    細胞工学   1995

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  • ヒト免疫不全ウイルス (HIV) の制御遺伝子の機能

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    蛋白質核酸酵素   40 ( 9 )   p1079 - 1091   1995

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    Other Link: http://search.jamas.or.jp/link/ui/1996001056

  • HIV遺伝子の構造と機能

    川村名子, 酒井博幸, 足立昭夫

    日本臨床増刊号   1993

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    Language:Japanese   Publishing type:Article, review, commentary, editorial, etc. (trade magazine, newspaper, online media)  

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  • HIVの制御遺伝子と遺伝子治療. エイズー基礎から臨床へ

    川村名子, 酒井博幸, 足立昭夫

    臨床医のための実験医学シリーズ12   1993

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  • AIDSウイルスーその増殖機構をめぐって

    川村名子, 酒井博幸, 足立昭夫

    感染症   1993

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

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  • HIVの起源

    足立昭夫, 酒井幸博, 川村名子

    Mebio   1993

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  • レトロウイルス

    酒井博幸, 川村名子, 足立昭夫

    化学工業   1993

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  • ヒト免疫不全ウイルス(HIV) の生物学.

    酒井博幸, 川村名子, 桜木小百合, 岩谷靖雅, 足立昭夫

    治療   1993

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  • HIV-1の増殖機構

    酒井博幸, 川村名子, 桜木小百合, 桜木淳一, 足立昭夫

    Minophagen Medical Review   1993

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Presentations

  • Patients with anti-MOG antibody-positive optic neuritis demonstrated characteristic clinical features and certain binding epitope on human MOG extracellular domain

    Tanaka K, Kawamura M, Koike N, Oone M, Sakimura K, Kezuka T, Ishikawa H

    ECTRIMS  2018.10 

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  • Progress of genetically modified mice for A3 group Invited International conference

    Kawamura Meiko

    Coference on Autophagy at Niigata University  2018.3 

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    Language:English   Presentation type:Oral presentation (general)  

    Venue:Niigata University  

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  • Exploring the epitopes of anti-MOG antibodies in the patients with inflammatory demyelinating disease presenting various clinical phenotypes International conference

    Naoto Koike, Meiko Kawamura, Moe Oono, Kenji Sakimura, Keiko Tanaka

    World Congress of Neurology  2017 

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  • デルタ型グルタミン酸受容体サブユニット機能とその量的関連

    中本 千尋, 川村 名子, 夏目 里恵, 阿部 学, 渡辺 雅彦, 崎村 建司

    日本生物学的神経医学会  2016 

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  • インターロイキン1によるグルタミン酸トランスポーターの発現調節ー脳内炎症におけるグリア細胞の役割を考察する Invited

    川村 名子

    京都大学ウイルス研究所 学術セミナー  2005.12  京都大学ウイルス研究所

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  • インターロイキン1によるグリア細胞の機能的変換

    川村 名子, 武井 延之, 那波 ひろゆき

    第70回 日本インターフェロン・サイトカイン学会  2005.6 

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  • 転写因子NF-kBを介したインターロイキン1によるグリア細胞の機能変化

    川村 名子, 武井 延之, 那波 宏之

    神経化学会  2004.8 

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  • 脳に高発現する膜結合型、新規ユビキチンライゲース(Momo及びSakura)の生化学的解析

    川村 名子, 荒木 一明, 鈴木 俊顕, 松田 憲之, 神辺 太樹, 千葉 智樹, 田中 啓二, 那波 宏之

    神経化学会  2003.8 

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  • 神経細胞とグリア細胞で同定されたZnフィンガー/RINGフィンガー含有分子、MomoとSakura

    荒木 一明, 川村 名子, 神辺 太樹, 石井 京子, 市川 富夫, 熊西 敏郎, 田中 啓二, 武井 延之, 那波 宏之

    神経化学会  2003.8 

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  • The surface expression of AMPA receptor is regulated by BDNF through the modulation of NSF-GluR2 interaction. International conference

    Narisawa-Saito M, Iwakura Y, Kawamura M, Araki K, Hussam J, Takei N, Nawa H

    31st Annual Meeting, Society for Neuroscience, San Diego, CA. USA  2001.11 

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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

    神経化学会  2001.9 

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  • Sindbis virus-mediated expression of Ca2+-permeable AMPA receptors in CA1 hippocampal neurons and induction of NMDA receptor-independent long-term poteintiation. International conference

    Kakegawa W, Okada T, Iino M, Yamada N, Tsuzuki K, Kawamura M, Nawa H, Ozawa S

    30th Annual Meeting, Society for Neuroscience, New Orleans, LA. USA  2000.11 

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  • Sindbis virus vector carrying GFP as a reporter gene: electrophysilogical and cell biological evaluation in the neocortical neuron. International conference

    Namba H, Kawamura M, Okada M, Otsu Y, Nawa H

    29th Annual Meeting, Society for Neuroscience, Miami Beach, FL. USA  1999.10 

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  • RNAウイルスベクターを用いた中枢神経細胞への遺伝子導入

    難波 寿明, 川村 名子, 岡田 誠剛, 大津 洋, 那波 宏之

    日本神経科学大会  1999.7 

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  • Functional analysis of HIV-1 gag proteins International conference

    Kawamura, M, Kitamura, T, Ishimoto, A, Adachi, A

    10th International Conference on AIDS Yokohama, Japan.  1994.8 

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  • Production of chimeric virus-like particles containing the HIV-1 gag/pol and HIV-2 gag gene products. International conference

    Kawamura, M, Shioda, T, Kitamura, T, Iwakura, Y, Shibuta, H

    8th International Conference on AIDS Amsterdam, Netherlands  1992.7 

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  • グレイマンガベイからのサル免疫不全ウイルス(SIV)の分離とその性状解析

    朝長 啓造, 片平 じゅん, Hassan MA, 川村 名子, 三浦 智行, 速水 正憲

    日本獣医学会学術集会  1991.3 

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  • Isolation of a highly divergent HIV-2 distinct from known isolates of HIV-2 and SIV. International conference

    Kawamura, M, Sakuragi, J, Fukasawa, M, Miura, T, Gojobori, T, Moriyama, E.N, Mingle, J.A.A, Netty, V.B.A, Hayami, M

    6th International Conference on AIDS San Francisco, USA  1990.6 

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  • Isolation and Characterization of HIV-2 from AIDS patient in Ghana International conference

    Ishikawa, K, Tsujimoto, H, Hasegawa, A, Miki, K, Mingle, J.A, Kawamura M, Hayami M

    4th International Conference on ADIS Stockholm, Sweden1988  1988.6 

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  • カモ由来ニューカッスル病ウイルスのニワトリヒナに対する病原性

    川村 名子

    日本獣医学会学術集会  1985.3 

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Industrial property rights

  • 血液を用いた統合失調症の診断方法

    那波 宏之, 染矢 俊幸, 村竹 辰之, 川村 名子

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    Application no:特開2003-334170  Date applied:2003.9

    Publication no:特願2004-135667  Date published:2004.5

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  • 精神分裂病により発現量が変化する遺伝子を規定する核酸を解析する方法

    那波 宏之, 高橋 均, 入谷 修司, 川村 名子

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    Application no:特願2002-036937  Date applied:2002.2

    Publication no:特開2003-235557  Date published:2003.8

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Research Projects

  • 遺伝子組み換えマウスの作製

    2010.4

    System name:科学研究費補助金

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    Grant type:Competitive

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  • 統合失調症関連遺伝子の探索と生化学的解析

    1998.6 - 2007.3

    System name:科学技術振興調整費

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    Grant type:Competitive

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  • 霊長類由来レトロウイルスの分子遺伝学

    1987.10 - 1995.3

    System name:科学研究費補助金

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    Grant type:Competitive

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  • 野生カモ類由来パラミキソウイルスのニワトリへの病原性と免疫原性について

    1983.4 - 1985.3

    System name:科学研究費補助金

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    Grant type:Competitive

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Teaching Experience (researchmap)