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Yu-ichi Goto

Researcher at University of Tsukuba

Publications -  267
Citations -  14997

Yu-ichi Goto is an academic researcher from University of Tsukuba. The author has contributed to research in topics: Mitochondrial DNA & Mitochondrial myopathy. The author has an hindex of 52, co-authored 244 publications receiving 13849 citations. Previous affiliations of Yu-ichi Goto include Hokkaido University.

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A mutation in the tRNA Leu(UUR) gene associated with the MELAS subgroup of mitochondrial encephalomyopathies

TL;DR: An A-to-G transition mutation at nucleotide pair 3,243 in the dihydrouridine loop of mitochondrial tRNALeu(UUR) that is specific to patients with MELAS is reported, which creates an Apal restriction site and could perform a simple molecular diagnostic test for the disease.
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Mitochondrial fission factor Drp1 is essential for embryonic development and synapse formation in mice

TL;DR: Drp1−/− murine embryonic fibroblasts and embryonic stem cells revealed that Drp1 is required for a normal rate of cytochrome c release and caspase activation during apoptosis, although mitochondrial outer membrane permeabilization, as examined by the release of Smac/Diablo and Tim8a, may occur independently of Drp 1 activity.
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Hydrogen sulfide increases glutathione production and suppresses oxidative stress in mitochondria.

TL;DR: H(2)S enhances the transport of cysteine to increase GSH production more than cystine transport and to redistribute the localization of GSH to mitochondria and provides a new mechanism of neuroprotection from oxidative stress by H( 2)S.
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A subtype of diabetes mellitus associated with a mutation of mitochondrial DNA

TL;DR: Diabetes mellitus associated with the A-->G mutation at position 3243 of mitochondrial leucine transfer RNA represents a subtype of diabetes found in both patients with IDDM and patients with NIDDM in Japan.
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Introduction of disease-related mitochondrial DNA deletions into HeLa cells lacking mitochondrial DNA results in mitochondrial dysfunction.

TL;DR: It is suggested that large-scale deletion mutations of mtDNA alone are sufficient for the mitochondrial dysfunction characteristic of CPEO.