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Naoto Ito

Researcher at Gifu University

Publications -  109
Citations -  3784

Naoto Ito is an academic researcher from Gifu University. The author has contributed to research in topics: Rabies virus & Virus. The author has an hindex of 34, co-authored 92 publications receiving 3164 citations. Previous affiliations of Naoto Ito include University of Massachusetts Medical School & Harvard University.

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Severe acute respiratory syndrome coronavirus nsp1 protein suppresses host gene expression by promoting host mRNA degradation.

TL;DR: expression of nsp1, the most N-terminal gene 1 protein, prevented Sendai virus-induced endogenous IFN-β mRNA accumulation without inhibiting dimerization of IFN regulatory factor 3, a protein that is essential for activation of theIFN- β promoter.
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Improved Recovery of Rabies Virus from Cloned cDNA Using a Vaccinia Virus‐Free Reverse Genetics System

TL;DR: A BHK cell clone is established that stably expresses T7 RNA polymerase, which is named BHK/T7–9 and recombinant rabies virus was efficiently recovered from the cloned cDNA.
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Dissecting the Causal Mechanism of X-Linked Dystonia-Parkinsonism by Integrating Genome and Transcriptome Assembly

TL;DR: The integrated genome and transcriptome assembly technologies suggest an SVA-mediated aberrant transcriptional mechanism associated with XDP and may provide a roadmap for layered technologies and integrated assembly-based analyses for other unsolved Mendelian disorders.
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Torsin mediates primary envelopment of large ribonucleoprotein granules at the nuclear envelope.

TL;DR: The cellular machinery underlying the exit of megaRNPs via budding is established, an explanation for the "nuclear blebbing" phenotype found in dystonia models is offered, and an important link between Torsin and the synaptic phenotypes observed in Dystonia is provided.
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Severe Acute Respiratory Syndrome Coronavirus 3a Protein Is a Viral Structural Protein

TL;DR: The association of a severe acute respiratory syndrome coronavirus (SCoV) accessory protein, 3a, with plasma membrane and intracellular SCoV particles in infected cells was shown, establishing that 3a protein was a SCoVs structural protein.