I. Ogiwara

发表

Altered hippocampal replay is associated with memory impairment in mice heterozygous for the Scn2a gene

Steven J. Middleton, K. Yamakawa, Steven J Middleton, 2018, Nature Neuroscience.

Nav1.1 Localizes to Axons of Parvalbumin-Positive Inhibitory Interneurons: A Circuit Basis for Epileptic Seizures in Mice Carrying an Scn1a Gene Mutation

Hiroyuki Miyamoto, Yuchio Yanagawa, Teiichi Furuichi, 2007, The Journal of Neuroscience.

Role of the C-Terminal Domain of RNA Polymerase II in U2 snRNA Transcription and 3′ Processing

A. Weiner, I. Ogiwara, E. Jacobs, 2004, Molecular and Cellular Biology.

SCN1A Mutation Mosaicism in a Family with Severe Myoclonic Epilepsy in Infancy

K. Yamakawa, Keiko Nakamura, M. Morimoto, 2006, Epilepsia.

De novo mutations of voltage-gated sodium channel αII gene SCN2A in intractable epilepsies

K. Yamakawa, T. Hashikawa, H. Osaka, 2009, Neurology.

Patients with a sodium channel alpha 1 gene mutation show wide phenotypic variation

K. Yamakawa, N. Yasui-Furukori, H. Osaka, 2007, Epilepsy Research.

Sodium channel dysfunction in intractable childhood epilepsy with generalized tonic–clonic seizures

K. Yamakawa, A. George, I. Ohmori, 2005, The Journal of physiology.

A homozygous mutation of voltage‐gated sodium channel βI gene SCN1B in a patient with Dravet syndrome

K. Yamakawa, Y. Inoue, S. Tsuchiya, 2012, Epilepsia.

Different degrees of loss of function between GEFS+ and SMEI Nav1.1 missense mutants at the same residue induced by rescuable folding defects

K. Yamakawa, Y. Ugawa, I. Ogiwara, 2012, Epilepsia.

Singular localization of sodium channel β4 subunit in unmyelinated fibres and its role in the striatum

F. Fujiyama, T. Kaneko, K. Yamakawa, 2014, Nature Communications.

Effect of ooplast activation on the development of oocytes following nucleus transfer in cattle.

Y. Sotomaru, T. Kono, I. Ogiwara, 1994, Theriogenology.

Retropositional parasitism of SINEs on LINEs: identification of SINEs and LINEs in elasmobranchs.

N Okada, M. Miya, N. Okada, 1999, Molecular biology and evolution.

V-SINEs: a new superfamily of vertebrate SINEs that are widespread in vertebrate genomes and retain a strongly conserved segment within each repetitive unit.

M. Miya, N. Okada, K. Ohshima, 2002, Genome research.

SINEs and LINEs share common 3' sequences: a review.

N. Okada, K. Ohshima, I. Ogiwara, 1997, Gene.

Scn1a mice exhibit hyperactivity, autism-like behavioral deficits and learning impairments

K. Yamakawa, Kazuyuki Yamada, I. Ogiwara, 2010, Neuroscience Research.

Nav1.2 haplodeficiency in excitatory neurons causes absence-like seizures in mice

Y. Yanagawa, K. Yamakawa, S. Itohara, 2018, Communications Biology.

Nav1.1 haploinsufficiency in excitatory neurons ameliorates seizure-associated sudden death in a mouse model of Dravet syndrome

N. Tamamaki, Y. Yanagawa, K. Yamakawa, 2013, Human molecular genetics.

Mouse with Nav1.1 haploinsufficiency, a model for Dravet syndrome, exhibits lowered sociability and learning impairment

K. Yamakawa, T. Hensch, M. Ōsawa, 2013, Neurobiology of Disease.

Deletions of SCN1A 5′ genomic region with promoter activity in Dravet syndrome

K. Yamakawa, H. Osaka, K. Haginoya, 2010, Human mutation.

Scn2a haploinsufficient mice display a spectrum of phenotypes affecting anxiety, sociability, memory flexibility and ampakine CX516 rescues their hyperactivity

K. Yamakawa, S. Itohara, T. Miyakawa, 2019, Molecular Autism.

A Kv4.2 truncation mutation in a patient with temporal lobe epilepsy

Kazumi Matsuda, Yushi Inoue, Koichi Baba, 2006, Neurobiology of Disease.

Involvement of the C‐terminal domain in cell surface localization and G‐protein coupling of mGluR6

Mie Gangi, Toshiyuki Ishii, T. Akagi, 2020, Journal of neurochemistry.

Impaired cortico-striatal excitatory transmission triggers epilepsy

K. Yamakawa, S. Itohara, T. Hensch, 2019, Nature Communications.

Scn1a-GFP transgenic mouse revealed Nav1.1 expression in neocortical pyramidal tract projection neurons

K. Yamakawa, S. Itohara, T. Tatsukawa, 2023, bioRxiv.

Impairments in social novelty recognition and spatial memory in mice with conditional deletion of Scn1a in parvalbumin-expressing cells

K. Yamakawa, T. Tatsukawa, I. Ogiwara, 2018, Neurobiology of Disease.

Altered Cardiac Electrophysiology and SUDEP in a Model of Dravet Syndrome

Brittany C. Clawson, K. Yamakawa, J. Parent, 2013, PloS one.

Nav1.2 is expressed in caudal ganglionic eminence-derived disinhibitory interneurons: Mutually exclusive distributions of Nav1.1 and Nav1.2.

Y. Yanagawa, K. Yamakawa, I. Ogiwara, 2017, Biochemical and biophysical research communications.

Altered hippocampal replay is associated with memory impairment in mice heterozygous for the Scn2a gene

Steven J. Middleton, K. Yamakawa, T. McHugh, 2018, Nature Neuroscience.

CRISPR/dCas9-based Scn1a gene activation in inhibitory neurons ameliorates epileptic and behavioral phenotypes of Dravet syndrome model mice

K. Yamakawa, S. Itohara, T. Hensch, 2020, Neurobiology of Disease.

The intracellular C-terminal domain of mGluR6 contains ER retention motifs

T. Akagi, I. Ogiwara, M. Kaneda, 2023, Molecular and Cellular Neuroscience.

Efficacy of stiripentol in hyperthermia‐induced seizures in a mouse model of Dravet syndrome

K. Yamakawa, Y. Inoue, Yukitoshi Takahashi, 2012, Epilepsia.

Impaired cortico-striatal excitatory transmission triggers epilepsy

K. Yamakawa, S. Itohara, T. Hensch, 2019, Nature Communications.

Acute Encephalopathy in a Patient with Dravet Syndrome

K. Yamakawa, H. Osaka, A. Okumura, 2011, Neuropediatrics.

[18F]fluorodeoxyglucose-positron emission tomography study of genetically confirmed patients with Dravet syndrome

K. Yamakawa, M. Ishitobi, K. Haginoya, 2018, Epilepsy Research.

Nav1.2 haplodeficiency in excitatory neurons causes absence-like seizures in mice

Y. Yanagawa, K. Yamakawa, S. Itohara, 2018, Communications Biology.

Nav1.2 is expressed in caudal ganglionic eminence-derived disinhibitory interneurons: Mutually exclusive distributions of Nav1.1 and Nav1.2.

Y. Yanagawa, K. Yamakawa, I. Ogiwara, 2017, Biochemical and biophysical research communications.