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Naoki Suzuki

Researcher at Tohoku University

Publications -  298
Citations -  11838

Naoki Suzuki is an academic researcher from Tohoku University. The author has contributed to research in topics: Amyotrophic lateral sclerosis & Haptic technology. The author has an hindex of 33, co-authored 282 publications receiving 9969 citations. Previous affiliations of Naoki Suzuki include Howard Hughes Medical Institute & Samsung.

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Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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Mutations of optineurin in amyotrophic lateral sclerosis

Hirofumi Maruyama, +28 more
- 13 May 2010 - 
TL;DR: It is shown that there are mutations in the gene encoding optineurin (OPTN), earlier reported to be a causative gene of primary open-angle glaucoma (POAG), in patients with ALS and these findings strongly suggest that OPTN is involved in the pathogenesis of ALS.
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High-energy long-cycling all-solid-state lithium metal batteries enabled by silver–carbon composite anodes

Yonggun Lee, +15 more
- 09 Mar 2020 - 
TL;DR: In this paper, a high performance all-solid-state lithium metal battery with a sulfide electrolyte is enabled by a Ag-C composite anode with no excess Li.
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Design and synthesis of the superionic conductor Na10SnP2S12.

William D. Richards, +11 more
- 17 Mar 2016 - 
TL;DR: This work reports the computation-assisted discovery and synthesis of a high-performance solid-state electrolyte material: Na10SnP2S12, with room temperature ionic conductivity rivalling the conductivity of the best sodium sulfide solid electrolytes to date.
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Loss-of-function mutations in the C9ORF72 mouse ortholog cause fatal autoimmune disease

Aaron Burberry, +30 more
- 13 Jul 2016 - 
TL;DR: It is shown that mice harboring loss-of-function mutations in the ortholog of C9ORF72 develop splenomegaly, neutrophilia, thrombocytopenia, increased expression of inflammatory cytokines, and severe autoimmunity, ultimately leading to a high mortality rate.