Kazunori Nakajima

ORCID: 0000-0003-1864-9425
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About
Contact & Profiles
Research Areas
  • Neurogenesis and neuroplasticity mechanisms
  • Axon Guidance and Neuronal Signaling
  • Neuroscience and Neuropharmacology Research
  • RNA Research and Splicing
  • MicroRNA in disease regulation
  • Hematopoietic Stem Cell Transplantation
  • Microtubule and mitosis dynamics
  • Blood donation and transfusion practices
  • Genetics and Neurodevelopmental Disorders
  • Blood groups and transfusion
  • Blood transfusion and management
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Genetic Syndromes and Imprinting
  • Immune Cell Function and Interaction
  • T-cell and B-cell Immunology
  • Bone health and treatments
  • Congenital heart defects research
  • Phosphodiesterase function and regulation
  • Organ Donation and Transplantation
  • Pluripotent Stem Cells Research
  • Bone and Joint Diseases
  • Neural dynamics and brain function
  • Genomics and Chromatin Dynamics
  • Cellular transport and secretion
  • Neonatal and fetal brain pathology

Keio University
2016-2025

Keio University Hospital
2011-2024

Nagasaki University
2008-2023

National Cerebral and Cardiovascular Center
2023

Toyama University Hospital
2023

Japanese Red Cross Society, Japan
2013-2022

Kouseiren Takaoka Hospital
2017-2021

National Medical and Surgical Center named after N.I. Pirogov
2020

The University of Tokyo
1987-2015

Tohoku University
2009-2015

Neural precursor cells (NPCs) have the ability to self-renew and give rise neuronal glial lineages. The fate decision of NPCs between proliferation differentiation determines number differentiated size each region brain. However, signals that regulate timing remain unclear. Here, we show Wnt signaling inhibits self-renewal capacity mouse cortical NPCs, instructively promotes their differentiation. Overexpression Wnt7a or a stabilized form beta-catenin in NPC cultures induced even presence...

10.1242/dev.01165 article EN Development 2004-05-18

Two distinct modes of radial neuronal migration, locomotion and somal translocation, have been reported in the developing cerebral cortex. Although these two migration well documented, cortical intermediate zone contains abundant multipolar cells, they do not resemble cells migrating by or translocation. Here, we report that express markers extend multiple thin processes various directions independently glial fibers. Time-lapse analysis living slices revealed any fixed cell polarity, very...

10.1523/jneurosci.23-31-09996.2003 article EN cc-by-nc-sa Journal of Neuroscience 2003-11-05

The neurological mouse mutant strain reeler displays abnormal laminar organization of several brain structures as a consequence defect in cell migration during neurodevelopment. This phenotype is result the disruption reelin , gene encoding protein that has structural characteristics extracellular matrix proteins. To understand molecular basis action Reelin on neuronal migration, we constructed full-length clone and used it to direct expression. Here, demonstrate secreted glycoprotein highly...

10.1523/jneurosci.17-01-00023.1997 article EN cc-by-nc-sa Journal of Neuroscience 1997-01-01

ABSTRACT Mutation of either reelin (Reln) or disabled-1 (Dab1) results in widespread abnormalities laminar structures throughout the brain and ataxia reeler scrambler mice. Both exhibit same neuroanatomical defects, including cerebellar hypoplasia with Purkinje cell ectopia disruption neuronal layers cerebral cortex hippocampus. Despite these phenotypic similarities, Reln Dab1 have distinct molecular properties. is a large extracellular protein secreted by Cajal-Retzius cells forebrain...

10.1242/dev.125.18.3719 article EN Development 1998-09-15

While the cortical interneurons derived from medial ganglionic eminence (MGE) migrate rather diffusely into cortex, that out caudal (CGE) mainly move caudally cerebral cortex and hippocampus in form of migratory stream (CMS) (Yozu et al., 2005). Although transplantation experiments at embryonic day 13.5 had revealed migrating cells these two populations are already intrinsically different regard to their ability respond CGE environment 2005), it is not known how specified behavior...

10.1523/jneurosci.2132-08.2008 article EN cc-by-nc-sa Journal of Neuroscience 2008-12-10

The mammalian cerebral cortex consists of six layers that are generated via coordinated neuronal migration during the embryonic period. Recent studies identified specific phases radial cortical neurons. After final division, neurons transform from a multipolar to bipolar shape within subventricular zone-intermediate zone (SVZ-IZ) and then migrate along glial fibres. Mice lacking Cdk5 exhibit abnormal corticogenesis owing defects. When we introduced GFP into migrating at E14.5 by in utero...

10.1242/dev.02854 article EN Development 2007-05-17

The expansion of the GGGGCC hexanucleotide repeat in non-coding region chromosome 9 open-reading frame 72 (C9orf72) gene is most common cause frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) (c9FTD/ALS). Recently, it was reported that an unconventional mechanism repeat-associated non-ATG (RAN) translation arises from C9orf72 expansion. Sense anti-sense transcripts expanded repeat, i.e. dipeptide protein (DRP) glycine–alanine (poly-GA), glycine–proline (poly-GP),...

10.1093/hmg/ddu576 article EN Human Molecular Genetics 2014-11-14

Mammalian neocortex has a laminated structure that develops in birth-date-dependent “inside-out” pattern. This layered is established by neuronal migration with sequential changes of the migratory mode regulated several signaling cascades, including Reelin–Disabled homolog 1 (Dab1) pathway. Although importance “locomotion,” major mode, been well established, physiological significance change from locomotion to “terminal translocation,” final unknown. In this study, we found outermost region...

10.1523/jneurosci.0650-11.2011 article EN Journal of Neuroscience 2011-06-22

Small axons far outnumber larger fibers in the corticospinal tract, but function of these small remains poorly understood. This is because they are difficult to identify, and therefore their physiology obscure. To assess extent mismatch between anatomic physiological measures, we compared conduction time velocity a large number macaque neurons with distribution axon diameters at level medullary pyramid, using both light electron microscopy. At microscopic level, total 4,172 were sampled from...

10.1152/jn.00720.2013 article EN cc-by Journal of Neurophysiology 2014-05-29
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