D-Index & Metrics Best Publications

D-Index & Metrics D-index (Discipline H-index) only includes papers and citation values for an examined discipline in contrast to General H-index which accounts for publications across all disciplines.

Discipline name D-index D-index (Discipline H-index) only includes papers and citation values for an examined discipline in contrast to General H-index which accounts for publications across all disciplines. Citations Publications World Ranking National Ranking
Genetics D-index 64 Citations 18,262 287 World Ranking 1974 National Ranking 72

Overview

What is he best known for?

The fields of study he is best known for:

  • Gene
  • Mutation
  • Internal medicine

Genetics, Mitochondrial DNA, Mitochondrion, Mitochondrial myopathy and Molecular biology are his primary areas of study. He focuses mostly in the field of Mitochondrial DNA, narrowing it down to matters related to Phenotype and, in some cases, DNA. The various areas that Yu-ichi Goto examines in his Mitochondrion study include RNA interference and Transcription.

His Mitochondrial myopathy research includes themes of Lactic acidosis, Internal medicine, Heteroplasmy and Mutation. His Lactic acidosis study which covers Encephalopathy that intersects with Pathology. His studies deal with areas such as Chromatin immunoprecipitation, Myopathy, MECP2 and Gene, Rett syndrome as well as Molecular biology.

His most cited work include:

  • A mutation in the tRNA Leu(UUR) gene associated with the MELAS subgroup of mitochondrial encephalomyopathies (1611 citations)
  • Mitochondrial fission factor Drp1 is essential for embryonic development and synapse formation in mice (718 citations)
  • Introduction of disease-related mitochondrial DNA deletions into HeLa cells lacking mitochondrial DNA results in mitochondrial dysfunction. (466 citations)

What are the main themes of his work throughout his whole career to date?

Yu-ichi Goto spends much of his time researching Genetics, Mitochondrial DNA, Internal medicine, Pathology and Molecular biology. His Gene, Mutation, Point mutation, Heteroplasmy and Mutation investigations are all subjects of Genetics research. His research in Mitochondrial DNA intersects with topics in Mitochondrion, Cytochrome c oxidase and Mutant.

In his study, Myopathy is strongly linked to Endocrinology, which falls under the umbrella field of Internal medicine. His studies in Pathology integrate themes in fields like Cortical dysplasia, White matter, Cerebellar ataxia and Kearns–Sayre syndrome. His Mitochondrial myopathy research is multidisciplinary, incorporating elements of Encephalopathy and Mitochondrial encephalomyopathy.

He most often published in these fields:

  • Genetics (37.31%)
  • Mitochondrial DNA (29.23%)
  • Internal medicine (23.08%)

What were the highlights of his more recent work (between 2014-2021)?

  • Genetics (37.31%)
  • Internal medicine (23.08%)
  • Gene (15.77%)

In recent papers he was focusing on the following fields of study:

His main research concerns Genetics, Internal medicine, Gene, Cell biology and Mitochondrion. He integrates Genetics and Pelizaeus Merzbacher like disease in his studies. His biological study spans a wide range of topics, including Gastroenterology, STIM1 and Endocrinology.

His Cell biology research integrates issues from Muscle disorder, Mutation, Protein biosynthesis, Muscular dystrophy and TRNA modification. His Mitochondrion study also includes fields such as

  • Mitochondrial disease, which have a strong connection to Mitochondrial myopathy, Lactic acidosis, RNA and Bicarbonate,
  • Induced pluripotent stem cell, Pentose phosphate pathway, Heteroplasmy and Mutant most often made with reference to Oxidative phosphorylation. His studies deal with areas such as Oxidative stress and Encephalopathy as well as Mitochondrial DNA.

Between 2014 and 2021, his most popular works were:

  • Dominant mutations in ORAI1 cause tubular aggregate myopathy with hypocalcemia via constitutive activation of store-operated Ca2+ channels (95 citations)
  • Higd1a is a positive regulator of cytochrome c oxidase (60 citations)
  • Plasma Metabolites Predict Severity of Depression and Suicidal Ideation in Psychiatric Patients-A Multicenter Pilot Analysis. (57 citations)

In his most recent research, the most cited papers focused on:

  • Gene
  • Mutation
  • Internal medicine

His primary scientific interests are in Genetics, Internal medicine, Mitochondrion, Gastroenterology and Molecular biology. Yu-ichi Goto frequently studies issues relating to White matter and Internal medicine. His Mitochondrion research includes themes of Oxidative phosphorylation, Heteroplasmy and Mitochondrial disease.

Yu-ichi Goto has researched Gastroenterology in several fields, including Odds ratio, Taurine, Cohort study and Cohort. The Molecular biology study combines topics in areas such as Compound heterozygosity, Pyruvate dehydrogenase complex and Induced pluripotent stem cell. His work in Cell biology tackles topics such as Endocrinology which are related to areas like Mutation.

This overview was generated by a machine learning system which analysed the scientist’s body of work. If you have any feedback, you can contact us here.

Best Publications

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

Yu-Ichi Goto;Ikuya Nonaka;Satoshi Horai.
Nature (1990)

2755 Citations

Mitochondrial fission factor Drp1 is essential for embryonic development and synapse formation in mice

Naotada Ishihara;Masatoshi Nomura;Akihiro Jofuku;Hiroki Kato.
Nature Cell Biology (2009)

1002 Citations

Hydrogen sulfide increases glutathione production and suppresses oxidative stress in mitochondria.

Yuka Kimura;Yu-Ichi Goto;Hideo Kimura.
Antioxidants & Redox Signaling (2010)

759 Citations

A subtype of diabetes mellitus associated with a mutation of mitochondrial DNA

T Kadowaki;H Kadowaki;Y Mori;K Tobe.
The New England Journal of Medicine (1994)

739 Citations

Introduction of disease-related mitochondrial DNA deletions into HeLa cells lacking mitochondrial DNA results in mitochondrial dysfunction.

Jun-Ichi Hayashi;Shigeo Ohta;Aiko Kikuchi;Masakazu Takemitsu.
Proceedings of the National Academy of Sciences of the United States of America (1991)

736 Citations

Inter-mitochondrial complementation: Mitochondria-specific system preventing mice from expression of disease phenotypes by mutant mtDNA

Kazuto Nakada;Kimiko Inoue;Kimiko Inoue;Tomoko Ono;Kotoyo Isobe.
Nature Medicine (2001)

573 Citations

Generation of mice with mitochondrial dysfunction by introducing mouse mtDNA carrying a deletion into zygotes

Kimiko Inoue;Kazuto Nakada;Atsuo Ogura;Kotoyo Isobe.
Nature Genetics (2000)

527 Citations

Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke‐like episodes (MELAS) A correlative study of the clinical features and mitochondrial DNA mutation

Y. Goto;S. Horai;T. Matsuoka;Y. Koga.
Neurology (1992)

515 Citations

Mutations in the integrin alpha7 gene cause congenital myopathy.

Yukiko K. Hayashi;Fan-Li Chou;Eva Engvall;Megumu Ogawa.
Nature Genetics (1998)

436 Citations

A new mtDNA mutation associated with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS).

Yu-ichi Goto;Ikuya Nonaka;Satoshi Horai.
Biochimica et Biophysica Acta (1991)

435 Citations

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