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Jae-Sung Kim

Researcher at University of Florida

Publications -  89
Citations -  12525

Jae-Sung Kim is an academic researcher from University of Florida. The author has contributed to research in topics: Mitochondrial permeability transition pore & Autophagy. The author has an hindex of 27, co-authored 82 publications receiving 10694 citations. Previous affiliations of Jae-Sung Kim include Washington University in St. Louis & University of North Carolina at Chapel Hill.

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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

Daniel J. Klionsky, +1287 more
- 01 Apr 2012 - 
TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy 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

Impaired autophagy: A mechanism of mitochondrial dysfunction in anoxic rat hepatocytes.

TL;DR: Calpain 2–mediated degradation of Atg7 and Beclin‐1 impairs mitochondrial autophagy, and this subsequently leads to MPT‐dependent hepatocyte death after A/R, which was reversed by nutrient depletion and adenoviral overexpression.
Journal ArticleDOI

Murine Cirrhosis Induces Hepatocyte Epithelial Mesenchymal Transition and Alterations in Survival Signaling Pathways

TL;DR: CLDH have increased vimentin and type 1 collagen expression and morphologic features consistent with EMT and, compared to NLDH, the cellular signaling phenotype of CLDH changes from a MAPK‐independent pathway to aMAPK‐dependent cell survival pathway.