Author

J.-I. Hayashi

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Cell Biology· 1 Pharmacology & Toxicology· 1

Signature Assays, Organisms & Methods

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Research Focus:cell signaling & trafficking· 2 Approach:experimental assay· 2 Assay:ATAC-seq· 1 Assay:bulk RNA-seq· 1 Research Focus:cancer & tumor microenvironment· 1 Organism:human· 1 Research Focus:metabolism & bioenergetics· 1 Assay:metabolomics· 1

Frequent Co-Authors

A. Okamoto· 1 shared C. Sumi· 1 shared E. Ogasawara· 1 shared H. Tanaka· 1 shared K. Hirota· 1 shared K. Nakada· 1 shared K. Nishi· 1 shared K. Takenaga· 1 shared

Activity by Year

2017-2019 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 24 mutual co-author links

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1 shared paperPharmacology & Toxicology

A. Okamoto

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2 papers

Recent·Most cited

Diabetic conditions induce intolerance to accumulation of pathogenic mitochondrial DNAs

E. Ogasawara, K. Nakada, S. Katada, T. Mito, J.-I. Hayashi

The paper shows diabetic conditions exacerbate mitochondrial respiration defects caused by pathogenic mtDNA mutations, suggesting diabetes may worsen mitochondrial diseases.

bioRxiv · Oct 2, 2019 · PreprintCell Biology

Propofol induces metabolic reprogramming and cell death in a mitochondrial electron transport chain-dependent manner

C. Sumi, A. Okamoto, H. Tanaka, K. Nishi, M. Kusunoki, T. Shoji, T. Uba, Y. Matsuo, T. Adachi, J.-I. Hayashi, K. Takenaga, K. Hirota

This study shows propofol causes metabolic reprogramming and cell death by impairing mitochondrial function, specifically complexes I and III, and this effect is exacerbated by preexisting mitochondrial dysfunction.

bioRxiv · Nov 16, 2017Pharmacology & Toxicology