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Gyesoon Yoon

Researcher at Ajou University

Publications -  63
Citations -  8335

Gyesoon Yoon is an academic researcher from Ajou University. The author has contributed to research in topics: Mitochondrion & Senescence. The author has an hindex of 30, co-authored 61 publications receiving 6918 citations.

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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.
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Mitochondria are impaired in the adipocytes of type 2 diabetic mice.

TL;DR: In this paper, the authors confirm a link between mitochondrial dysfunction and type 2 diabetes, and propose a method to confirm the link between mitochondria dysfunction and Type 2 diabetes using a blood test.
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Two distinct modes of cell death induced by doxorubicin: apoptosis and cell death through mitotic catastrophe accompanied by senescence-like phenotype.

TL;DR: Results indicate that different doses of doxorubicin activate different regulatory mechanisms to induce either apoptosis or cell death through mitotic catastrophe.
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Transcriptional regulation of autophagy by an FXR–CREB axis

TL;DR: It is shown that the fed-state sensing nuclear receptor farnesoid X receptor (FXR) and the fasting transcriptional activator cAMP response element-binding protein (CREB) coordinately regulate the hepatic autophagy gene network, resulting in sustained nutrient regulation of autophaky during feeding/fasting cycles.
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Formation of elongated giant mitochondria in DFO-induced cellular senescence: involvement of enhanced fusion process through modulation of Fis1.

TL;DR: It was found that direct induction of mitochondrial elongation by blocking mitochondrial fission process with Fis1‐ΔTM or Drp1‐K38A was sufficient to develop senescent phenotypes with increased ROS production, suggesting that mitochondria elongation may play an important role as a mediator in stress‐induced premature senescence.