Su Jin Yu
Korea University
6 Papers
63 Citations
Su Jin Yu is an academic researcher from Korea University. The author has contributed to research in topics: Cell cycle checkpoint & Cyclin-dependent kinase. The author has an hindex of 5, co-authored 5 publications.
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Papers
Glycogen Synthase Kinase 3β Phosphorylates p21WAF1/CIP1 for Proteasomal Degradation after UV Irradiation
TL;DR: GSK-3β is activated by UV irradiation through the ATR signaling pathway and phosphorylates p21 at ser-114 for its degradation by the proteasome, the first demonstration of GSK-3 β as the missing link between UV-induced ATR activation and p21 degradation.
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Panaxydol induces apoptosis through an increased intracellular calcium level, activation of JNK and p38 MAPK and NADPH oxidase-dependent generation of reactive oxygen species
TL;DR: Data indicate that panaxydol induces apoptosis preferentially in cancer cells, and the signaling mechanisms involve a [Ca2+]i increase, JNK and p38 MAPK activation, and ROS generation through NADPH oxidase and mitochondria.
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Induction of G1 cell cycle arrest and p27KIP1 increase by panaxydol isolated from Panax ginseng.
TL;DR: Results indicate that panaxydol induces G(1) cell cycle arrest by decreasing Cdk2 activity and up-regulating p27(KIP1) protein expression, and cycloheximide reversed the growth inhibition induced by panxydol and partially abrogated the increase in p 27(K IP1) expression.
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IL-4 inhibits proliferation of renal carcinoma cells by increasing the expression of p21WAF1 and IRF-1.
TL;DR: It is shown that IL-4 inhibits cell cycle progression at the G1 phase in Caki-1 cells by increasing the expression of p21WAF1 and interferon regulatory factor (IRF)-1, and decreasing the cyclin dependent kinase (CDK) 2 activity.
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The tRNA-Derived Fragment tRF-24-V29K9UV3IU Functions as a miRNA-like RNA to Prevent Gastric Cancer Progression by Inhibiting GPR78 Expression
TL;DR: It is suggested that the tRF-24-V29K9UV3IU/GPR78 axis serves as a potential therapeutic target in GC and functions as a miRNA-like fragment to suppress GPR78 expression and thus inhibit GC progression.
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