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Shin-ichi Muramatsu

Researcher at Jichi Medical University

Publications -  189
Citations -  6916

Shin-ichi Muramatsu is an academic researcher from Jichi Medical University. The author has contributed to research in topics: Dopamine & Adeno-associated virus. The author has an hindex of 40, co-authored 165 publications receiving 5972 citations. Previous affiliations of Shin-ichi Muramatsu include Meijo University & National Institutes of Health.

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Deletion of Class II ADP-Ribosylation Factors in Mice Causes Tremor by the Nav1.6 Loss in Cerebellar Purkinje Cell Axon Initial Segments

TL;DR: In this article, the authors found that decreasing the expression of class II ARF proteins, through the generation of ARF4+/-/ARF5-/- mice, impairs Nav1.6 immunoreactivity to the axon initial segment (AIS) of cerebellar Purkinje cells (PCs), thereby resulting in the impairment of action potential firing of PCs.
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Engineered adeno-associated virus 3 vector with reduced reactivity to serum antibodies.

TL;DR: In this article, triple mutant AAV3 (AAV.GT5) vector was generated by introducing three substitutions (S472A, S587A, and N706A) on the surface loop of AAV-3B capsid protein.
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Intra-cisterna magna delivery of an AAV vector with the GLUT1 promoter in a pig recapitulates the physiological expression of SLC2A1

TL;DR: Exogenous GLUT1 was mainly expressed in the endothelium, followed by glia and neurons, which was contrasted with the neuronal-predominant expression of GFP by the CMV promotor, which is considered to be a feasible approach for gene therapy ofGLUT1DS.
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Administration of tetrahydrobiopterin restored the decline of dopamine in the striatum induced by an acute action of MPTP.

TL;DR: The present data suggest that perturbation of the BH4 metabolism would be the cause of early and persistent dopamine depletion in the striatum of MPTP‐treated mice and suggest that MPTP perturbs the Bh4 metabolism in the DA neurons.
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Mutational and functional analysis of Glucose transporter I deficiency syndrome

TL;DR: Enzymatic photometric 2DG uptake study appears to be a suitable functional assay to predict the effect of SLC2A1 mutations on GLUT1 transport, correlated with disease severity.