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Neurochemistry(Partnership field)Neurochemistry

Introduction

 Laboratory of Neurochemistry has been founded in Research Institute for Developmental Disorders, Aichi Human Service Center, Kasugai-city, next to Nagoya-city. The institute consists of 7 research units, i.e., department of genetics, department of embryology, department of perinatology, department of molecular neurobiology, department of pathology, department of functioning science, and department of education and social service. These research units are altogether conducting wide varieties of research on developmental disorders. Thus a major aim of the laboratory is elucidating the mechanisms underlying developmental abnormalities, such like autism spectrum disorders and congenital and acquired intellectual disabilities, and developing new therapeutic strategies against developmental disorders. We are now focusing especially on several investigations using animal models, however, neuronal cell analyses utilizing human induced pluripotent stem (iPS) cells and clinical electro-physiological studies on patients are being conducted either.

Research Projects

  1. Pathophysiological analyses of causative genes for intellectual disability

    i) Comprehensive analyses in corticogenesis and pathophysiology of intellectual disability of a Mediator complex subunit, MED13L (Mediator Complex Subunit 13 like)
    ii) Comprehensive analyses of a heterotrimeric GTP-binding protein, Gi2, in the corticogenesis: Possible involvement in periventricular nodular heterotopia and intellectual disability

  2. Pathophysiological analyses of causative genes for autism-spectrum disorder

    i) Comprehensive analyses of RBFOX1, a causative gene for autism-spectrum disorder and other neurodevelopmental diseases, in the brain development
    ii) Comprehensive analyses of a circadian-relevant gene NR1D1 in brain development: possible involvement in the pathophysiology of autism spectrum disorders
    iii) Expression, transcriptional and posttranscriptional regulation, and functionalanalyses of NLGN4X in human brain.

  3. Development of stem cell therapies against mouse perinatal brain damage model.
  4. Pathophysiological studies on mouse models of dysmyelination.

Faculty Members

FacultyPositionDepartment
Atsuo Nakayama Chief, laboratory of embryology Institute for developmental disorder (Neurochemistry)
Koh-ichi Nagata Chief, laboratory of molecular neurobiology Institute for developmental disorder (Neurochemistry)

Bibliography

  • 2017
    1. Inoue M, Iwai R, Tabata H, Konno D, Komabayashi-Suzuki M, Watanabe C, Iwanari H, Mochizuki Y, Hamakubo T, Matsuzaki F, Nagata K, Mizutani K. Prdm16 is critical for progression of the multipolar phase during neural differentiation of the developing neocortex. Development, in press
    2. Goto M, Mizuno M, Matsumoto A, Yang Z, Jimbo FE, Tabata H, Yamagata T, Nagata K. Role of a circadian-relevant gene, NR1D1, in the brain development: possible involvement in the pathophysiology of autism spectrum disorders. Sci. Rep., 2017; 7: 43945.
    3. Hamada N, Negishi Y, Mizuno M, Miya F, Hattori A, Okamoto N, Kato M, Tsunoda T, Yamasaki M, Kanemura Y, Kosaki K, Tabata H, Saitoh S, Nagata K. Role of a heterotrimeric G-protein, Gi2, in the corticogenesis: Possible involvement in periventricular nodular heterotopia and intellectual disability. J. Neurochem., 2017; 140: 82-95.
  • 2016
    1. Inaguma Y, Matsumoto A, Noda M, Tabata H, Maeda A, Goto M, Usui D, Jimbo FE, Kikkawa K, Ohtsuki M, Momoi YM, Osaka H, Yamagata T, Nagata K. Role of Class III phosphoinositide 3-kinase in the brain development: possible involvement in specific learning disorders. J. Neurochem., 2016; 139: 245-255.
    2. Ito H, Morishita R, Nagata K. Schizophrenia susceptibility gene product dysbindin-1 regulates the homeostasis of cyclin D1. BBA-Molecular Basis of Disease, 2016; 1862: 1383-1391.
    3. Hamada N, Ito H, Nishijo T, Iwamoto I, Morishita R, Tabata H, Momiyama T, Nagata K. Essential role of the nuclear isoform of RBFOX1, a candidate gene for autism spectrum disorders, in the brain development. Sci. Rep., 2016; 6: 30805.
    4. Yang Z, Matsumoto A, Nakayama K, Jimbo FE, Kojima K, Nagata K, Iwamoto S, Yamagata T. Circadian-relevant genes are highly polymorphic in autism spectrum disorder patients. Brain & Dev., 2016; 38: 91-99.
    5. Yuan Q, Yang F, Xiao Y, Tan S, Husain N, Ren M, Hu Z, Martinowich K, Ng JS, Kim PJ, Han W, Nagata K, Weinberger DR, H. Je S. Regulation of BDNF exocytosis and GABAergic interneuron synapse by the schizophrenia susceptibility gene dysbindin-1. Biol. Psychiatry, 2016; 80: 312–322.
    6. Inaguma Y, Ito H, Iwamoto I, Matsumoto A, Yamagata T, Tabata H, Nagata K. Morphological characterization of Class III phosphoinositide 3-kinase during mouse brain development. Med. Mol. Morphol., 2016; 49(1): 28-33.
  • 2015
    1. Hamada N, Ito H, Iwamoto I, Morishita R, Tabata H, Nagata K. Role of the cytoplasmic isoform of RBFOX1/A2BP1 in establishing the architecture of the developing cerebral cortex. Mol. Autism, 2015; 6: 56.
    2. Lee SA, Kim SM, Suh BK, Sun HY, Park YU, Hong JH, Park C, Nguyen MD, Nagata K, Yoo JY, Park SK. Disrupted-in-schizophrenia 1 (DISC1) regulates dysbindin function by enhancing its stability. J. Biol. Chem., 2015; 290: 7087-7096.
    3. Inaguma Y, Ito H, Hara A, Iwamoto I, Matsumoto A, Yamagata T, Tabata H, Nagata K. Morphological characterization of mammalian Timeless in the mouse brain development. Neurosci. Res., 2015; 92: 21-28.
    4. Mizuno M, Matsumoto A, Hamada N, Ito H, Miyauchi A, Jimbo FE, Momoi YM, Tabata H, Yamagata T, Nagata K. Role of an adaptor protein Lin-7B in brain development: possible involvement in autism spectrum disorders. J. Neurochem., 2015; 132: 61-69.
  • 2014
    1. Ito H, Morishita R, Iwamoto I, Nagata K. Establishment of an in vivo electroporation method into postnatal newborn neurons in the dentate gyrus. Hippocampus, 2014; 24:1449-1457.
    2. Nishimura YV, Shikanai M, Hoshino M, Ohshima T, Nabeshima Y, Mizutani K, Nagata K, Nakajima K, Kawauchi T. Cdk5 and its substrates, Dcx and p27kip1, regulate cytoplasmic dilation formation and nuclear elongation in migrating neurons.Development, 2014; 141: 3540-3550.
    3. Matsumoto A, Mizuno M, Hamada N, Nozaki Y, Jimbo F E, Momoi Y M, Nagata K, Yamagata T. LIN7A depletion disrupts cerebral cortex development, contributing to intellectual disability in 12q21-deletion syndrome. PLOS ONE, 2014; 9(3): e92695.
    4. Tanabe K, Yamazaki H, Inaguma Y, Asada A, Kimura T, Takahashi J, Taoka M, Ohshima T, Furuichi T, Isobe T, Nagata K, Shirao T, Hisanaga S. Phosphorylation of Drebrin by cyclin-dependent kinase 5 and its role in neuronal migration. PLOS ONE, 2014; 9(3): e92291.
    5. Inaguma Y, Hamada N, Tabata H, Iwamoto I, Mizuno M, Nishimura VY, Ito H, Morishita R, Suzuki M, Ohno K, Kumagai T, Nagata K. SIL1, a causative cochaperone gene of Marinesco-Sjögren syndrome, plays an essential role in establishing the architecture of the developing cerebral cortex. EMBO Mol. Med., 2014; 6: 414–429.
    6. Mizutani Y, Iwamoto I, Kanoh H, Seishima M and Nagata K. Expression of Drebrin, an actin binding protein, in basal cell carcinoma, trichoblastoma and trichoepithelioma. Histol Histopathol., 2014; 29: 757-766.

Research Keywords

Autism spectrum disorders、Intellectual disability、Cerebral cortical development