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Young J. Oh

Researcher at Yonsei University

Publications -  132
Citations -  11902

Young J. Oh is an academic researcher from Yonsei University. The author has contributed to research in topics: Programmed cell death & Apoptosis. The author has an hindex of 40, co-authored 118 publications receiving 10084 citations. Previous affiliations of Young J. Oh include The Catholic University of America & Ajou University.

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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.
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

Minocycline reduces cell death and improves functional recovery after traumatic spinal cord injury in the rat.

TL;DR: Data suggest that minocycline treatment modulated expression of cytokines, attenuated cell death and the size of lesions, and improved functional recovery in the injured rat, suggesting that this approach may provide a therapeutic intervention enabling us to reduce cellDeath and improve functional recovery after SCI.
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Two distinct mechanisms are involved in 6-hydroxydopamine- and MPP+- induced dopaminergic neuronal cell death: Role of caspases, ROS, and JNK

TL;DR: The possibility that MPTP and 6‐hydroxydopamine act on distinct cell death pathways in a murine dopaminergic neuronal cell line is examined, finding that cells treated with 6‐OHDA accompanied ultrastructural changes typical of apoptosis, whereas MPP+ treatment induced necrotic manifestations.
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Proteotoxic Stress Induces Phosphorylation of p62/SQSTM1 by ULK1 to Regulate Selective Autophagic Clearance of Protein Aggregates

TL;DR: Proteotoxic stress imposed by the proteasome inhibition or expression of polyglutamine expanded huntingtin induces p62 phosphorylation at its ubiquitin-association (UBA) domain that regulates its binding to ubiquitinated proteins, suggesting a potential novel drug target for the treatment of proteinopathies including Huntington's disease.