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Yuzuru Imai

Researcher at Juntendo University

Publications -  119
Citations -  17022

Yuzuru Imai is an academic researcher from Juntendo University. The author has contributed to research in topics: Parkin & PINK1. The author has an hindex of 42, co-authored 111 publications receiving 14773 citations. Previous affiliations of Yuzuru Imai include Tohoku University & RIKEN Brain Science Institute.

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Journal ArticleDOI

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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A Serine Protease, HtrA2, Is Released from the Mitochondria and Interacts with XIAP, Inducing Cell Death

TL;DR: HtrA2 is a Smac-like inhibitor of IAP activity with a serine protease-dependent cell death-inducing activity, which is neither accompanied by a significant increase in caspase activity nor inhibited by casp enzyme inhibitors, including XIAP.
Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

Daniel J. Klionsky, +2983 more
- 08 Feb 2021 - 
TL;DR: In this article, the authors present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes.
Journal ArticleDOI

An Unfolded Putative Transmembrane Polypeptide, which Can Lead to Endoplasmic Reticulum Stress, Is a Substrate of Parkin

TL;DR: It is shown that the unfolded Pael receptor is a substrate of Parkin, the accumulation of which may cause selective neuronal death in AR-JP.
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Mitochondrial pathology and muscle and dopaminergic neuron degeneration caused by inactivation of Drosophila Pink1 is rescued by Parkin

TL;DR: It is shown that inhibition of Drosophila Pink1 function results in energy depletion, shortened lifespan, and degeneration of select indirect flight muscles and dopaminergic neurons, and the level of Parkin protein is significantly reduced in dPink1 RNA interference animals.