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Sung Bae Lee

Researcher at Daegu Gyeongbuk Institute of Science and Technology

Publications -  62
Citations -  5011

Sung Bae Lee is an academic researcher from Daegu Gyeongbuk Institute of Science and Technology. The author has contributed to research in topics: Ubiquitin & Proteasome. The author has an hindex of 21, co-authored 58 publications receiving 3616 citations. Previous affiliations of Sung Bae Lee include Dong-a University & KAIST.

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Mitochondrial dysfunction in Drosophila PINK1 mutants is complemented by parkin

TL;DR: The genetic evidence clearly establishes that Parkin and PINK1 act in a common pathway in maintaining mitochondrial integrity and function in both muscles and dopaminergic neurons.
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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.
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Parkin negatively regulates JNK pathway in the dopaminergic neurons of Drosophila

TL;DR: It is suggested that loss of Parkin function up-regulates the JNK signaling pathway, which may contribute to the vulnerability of dopaminergic neurons in Drosophila parkin mutants and perhaps autosomal recessive juvenile parkinsonism patients.
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Drosophila DJ-1 mutants show oxidative stress-sensitive locomotive dysfunction

TL;DR: The homozygous mutants showed severe defects in locomotor ability without loss of DA neurons, consistent with the previous mice DJ-1 mutant studies, and it was found that Drosophila DJs-1 is prominently localized in mitochondria, suggesting thatDJ-1 functions as a protector against oxidative stress in mitochondia.
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Activity of the mitochondrial calcium uniporter varies greatly between tissues

TL;DR: Surprisingly, heart mitochondria shows a dramatically lower MCU current density than the other tissues studied, and low MCU activity is likely essential to avoid cytosolic Ca2+ sink due to excessive mitochondrial Ca2- uptake.