S
Sung Eun Kim
Researcher at College of Health Sciences, Bahrain
Publications - 23
Citations - 1512
Sung Eun Kim is an academic researcher from College of Health Sciences, Bahrain. The author has contributed to research in topics: Programmed cell death & Autophagy. The author has an hindex of 13, co-authored 21 publications receiving 1151 citations. Previous affiliations of Sung Eun Kim include University of California & Cornell University.
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Journal ArticleDOI
Ultrasmall nanoparticles induce ferroptosis in nutrient-deprived cancer cells and suppress tumour growth
Sung Eun Kim,Li Zhang,Kai Ma,Michelle Riegman,Feng Chen,Irina Ingold,Marcus Conrad,Melik Z. Turker,Minghui Gao,Xuejun Jiang,Xuejun Jiang,Sebastien Monette,Mohan Pauliah,Mithat Gonen,Pat Zanzonico,Thomas P. Quinn,Ulrich Wiesner,Michelle S. Bradbury,Michael Overholtzer,Michael Overholtzer +19 more
TL;DR: It is shown that ultrasmall (< 10 nm in diameter) poly(ethylene glycol) (PEG)-coated silica nanoparticles, functionalized with melanoma-targeting peptides, can induce a form of programmed cell death known as ferroptosis in starved cancer cells and cancer-bearing mice.
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Autophagy machinery mediates macroendocytic processing and entotic cell death by targeting single membranes
Oliver Florey,Sung Eun Kim,Sung Eun Kim,Cynthia P. Sandoval,Cole M. Haynes,Cole M. Haynes,Michael Overholtzer,Michael Overholtzer +7 more
TL;DR: It is demonstrated that proteins of the autophagy pathway can target single-membrane vacuoles in cells in the absence of pathogenic organisms.
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V-ATPase and osmotic imbalances activate endolysosomal LC3 lipidation
TL;DR: Evidence is presented that this pathway requires activity of the vacuolar-type H+-ATPase (V- ATPase) and is induced by osmotic imbalances within endolysosomal compartments, and it is demonstrated that the widely and therapeutically used drug chloroquine, which is conventionally used to inhibit autophagy flux, is an inducer of LC3 lipidation.
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Direct and indirect contribution of human embryonic stem cell-derived hepatocyte-like cells to liver repair in mice
Dong Hun Woo,Suel Kee Kim,Suel Kee Kim,Hee Joung Lim,Jeonghoon Heo,Hyung Soon Park,Gum Yong Kang,Sung Eun Kim,Hyun Ju You,Daniel J. Hoeppner,Young Chul Kim,Heechung Kwon,Tae Hyun Choi,Joo Hee Lee,Su Hee Hong,Kang Won Song,Eun–Kyung Ahn,Josh G. Chenoweth,Paul J. Tesar,Ronald D.G. McKay,Jong-Hoon Kim +20 more
TL;DR: Hepatocyte-like cells derived from human embryonic stem cells contribute to recovery of injured liver tissues in mice, not only by cell replacement but also by delivering trophic factors that support endogenous liver regeneration.
Journal ArticleDOI
RIPK1-mediated induction of mitophagy compromises the viability of extracellular-matrix-detached cells.
Mark A. Hawk,Cassandra L. Gorsuch,Patrick Fagan,Chan Lee,Chan Lee,Sung Eun Kim,Sung Eun Kim,Jens C. Hamann,Joshua A. Mason,Kelsey J. Weigel,Matyas Abel Tsegaye,Luqun Shen,Sydney Shuff,Junjun Zuo,Stephan Hu,Lei Jiang,Sarah Chapman,W. Matthew Leevy,Ralph J. DeBerardinis,Michael Overholtzer,Michael Overholtzer,Zachary T. Schafer +21 more
TL;DR: RIPK1 activation during extracellular matrix detachment induces mitophagy through mitochondrial phosphatase PGAM5 to increase reactive oxygen species and non-apoptotic cell death, and that antagonizing RIPK1/PGAM5 enhances tumour formation in vivo.