Koh-ichi Nagata

Morphological characterization of mammalian timeless in the mouse brain development.

Morphological characterization of Class III phosphoinositide 3-kinase during mouse brain development.

Schizophrenia susceptibility gene product dysbindin-1 regulates the homeostasis of cyclin D1.

Role of Class III phosphoinositide 3-kinase in the brain development: possible involvement in specific learning disorders.

Autism spectrum disorder-associated genes and the development of dentate granule cells.

Expression analyses of Phactr1 (phosphatase and actin regulator 1) during mouse brain development.

MUNC18-1 gene abnormalities are involved in neurodevelopmental disorders through defective cortical architecture during brain development.

Expression analyses of Dusp22 (Dual-specificity phosphatase 22) in mouse tissues.

Functions of Rhotekin, an Effector of Rho GTPase, and Its Binding Partners in Mammals.

Role of Per3, a circadian clock gene, in embryonic development of mouse cerebral cortex.

Expression Analyses of POGZ, A Responsible Gene for Neurodevelopmental Disorders, during Mouse Brain Development.

Spatiotemporally Dependent Vascularization Is Differently Utilized among Neural Progenitor Subtypes during Neocortical Development.

Biochemical and morphological characterization of SEPT1 in mouse brain.

Neuropathophysiological significance of the c.1449T>C/p.(Tyr64Cys) mutation in the CDC42 gene responsible for Takenouchi-Kosaki syndrome.

Heterotrimeric G-protein, Gi1, is involved in the regulation of proliferation, neuronal migration, and dendrite morphology during cortical development in vivo.

Pogz deficiency leads to transcription dysregulation and impaired cerebellar activity underlying autism-like behavior in mice.

Expression analyses of PLEKHG2, a Rho family-specific guanine nucleotide exchange factor, during mouse brain development.

Expression Analyses of Mediator Complex Subunit 13-Like: A Responsible Gene for Neurodevelopmental Disorders during Mouse Brain Development.

Author Correction: Pogz deficiency leads to transcription dysregulation and impaired cerebellar activity underlying autism-like behavior in mice.

Physiological significance of WDR45, a responsible gene for β-propeller protein associated neurodegeneration (BPAN), in brain development.

The synaptic scaffolding protein CNKSR2 interacts with CYTH2 to mediate hippocampal granule cell development.

Expression Analyses of Rac3, a Rho Family Small GTPase, during Mouse Brain Development.

Pathophysiological Mechanisms in Neurodevelopmental Disorders Caused by Rac GTPases Dysregulation: What's behind Neuro-RACopathies.

Functions of CNKSR2 and Its Association with Neurodevelopmental Disorders.

Impaired Function of PLEKHG2, a Rho-Guanine Nucleotide-Exchange Factor, Disrupts Corticogenesis in Neurodevelopmental Phenotypes.

Expression Analyses of Cep152, a Responsible Gene Product for Autosomal Recessive Primary Microcephaly, during Mouse Brain Development.

Gain-of-function p.F28S variant in disrupts neuronal differentiation, migration and axonogenesis during cortical development, leading to neurodevelopmental disorder.

Variant-specific changes in RAC3 function disrupt corticogenesis in neurodevelopmental phenotypes.

Expression Analyses of Polo-Like Kinase 4, a Gene Product Responsible for Autosomal Recessive Microcephaly and Seckel Syndrome, during Mouse Brain Development.

Deficiency of , a gene related to intellectual disability, causes impaired neuronal development and a mild behavioural phenotype.

Erratic and blood vessel-guided migration of astrocyte progenitors in the cerebral cortex.

Pathophysiological Mechanism of Neurodevelopmental Disorders-Overview.

Expression Analyses of Rich2/Arhgap44, a Rho Family GTPase-Activating Protein, during Mouse Brain Development.

MED13L and its disease-associated variants influence the dendritic development of cerebral cortical neurons in the mammalian brain.

Histological Analysis of a Mouse Model of the 22q11.2 Microdeletion Syndrome.

A missense variant at the RAC1-PAK1 binding site of RAC1 inactivates downstream signaling in VACTERL association.

Expression analyses of WAC, a responsible gene for neurodevelopmental disorders, during mouse brain development.

Expression analysis of type I ARF small GTPases ARF1-3 during mouse brain development.