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Gang Min Hur

Researcher at Chungnam National University

Publications -  89
Citations -  12602

Gang Min Hur is an academic researcher from Chungnam National University. The author has contributed to research in topics: Apoptosis & Kinase. The author has an hindex of 30, co-authored 85 publications receiving 11029 citations. Previous affiliations of Gang Min Hur include National Institutes of Health & Korea Research Institute of Bioscience and Biotechnology.

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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

Tumor Necrosis Factor-induced Nonapoptotic Cell Death Requires Receptor-interacting Protein-mediated Cellular Reactive Oxygen Species Accumulation

TL;DR: This study utilized gene knockout mouse embryonic fibroblasts cells and found that tumor necrosis factor receptor (TNFR) I mediates TNF-induced necrotic cell death, and that RIP, FADD, and TRAF2 are critical components of the signaling cascade of this TNF/NVC cell death.
Journal ArticleDOI

Caffeic acid phenethyl ester inhibits nitric oxide synthase gene expression and enzyme activity.

TL;DR: Caffeic acid phenethyl ester may exert its anti-inflammatory effect by inhibiting the iNOS gene expression at the transcriptional level through the suppression of NF-kappaB activation, and by directly inhibited the catalytic activity of iNos.