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33 results on '"Kim, Choong Won"'

4. Identification of Growth Factors, Cytokines and Mediators Regulated by Artemisia annua L. Polyphenols (pKAL) in HCT116 Colorectal Cancer Cells: TGF-β1 and NGF-β Attenuate pKAL-Induced Anticancer Effects via NF-κB p65 Upregulation

Author

Jung, Eun Joo, primary, Paramanantham, Anjugam, additional, Kim, Hye Jung, additional, Shin, Sung Chul, additional, Kim, Gon Sup, additional, Jung, Jin-Myung, additional, Hong, Soon Chan, additional, Chung, Ky Hyun, additional, Kim, Choong Won, additional, and Lee, Won Sup, additional

Published
2022
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6. Artemisia annua L. Polyphenol-Induced Cell Death Is ROS-Independently Enhanced by Inhibition of JNK in HCT116 Colorectal Cancer Cells

Author

Jung, Eun Joo, primary, Paramanantham, Anjugam, additional, Kim, Hye Jung, additional, Shin, Sung Chul, additional, Kim, Gon Sup, additional, Jung, Jin-Myung, additional, Ryu, Chung Ho, additional, Hong, Soon Chan, additional, Chung, Ky Hyun, additional, Kim, Choong Won, additional, and Lee, Won Sup, additional

Published
2021
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7. p53 Enhances Artemisia annua L. Polyphenols-Induced Cell Death Through Upregulation of p53-Dependent Targets and Cleavage of PARP1 and Lamin A/C in HCT116 Colorectal Cancer Cells

Author

Jung, Eun Joo, primary, Lee, Won Sup, additional, Paramanantham, Anjugam, additional, Kim, Hye Jung, additional, Shin, Sung Chul, additional, Kim, Gon Sup, additional, Jung, Jin-Myung, additional, Ryu, Chung Ho, additional, Hong, Soon Chan, additional, Chung, Ky Hyun, additional, and Kim, Choong Won, additional

Published
2020
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8. Polyphenols Extracted from Artemisia annua L. Exhibit Anti-Cancer Effects on Radio-Resistant MDA-MB-231 Human Breast Cancer Cells by Suppressing Stem Cell Phenotype, β-Catenin, and MMP-9

Author

Ko, Young Shin, primary, Jung, Eun Joo, additional, Go, Se-il, additional, Jeong, Bae Kwon, additional, Kim, Gon Sup, additional, Jung, Jin-Myung, additional, Hong, Soon Chan, additional, Kim, Choong Won, additional, Kim, Hye Jung, additional, and Lee, Won Sup, additional

Published
2020
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17. The expression of ketohexokinase is diminished in human clear cell type of renal cell carcinoma

Author

Hwa, Jeong Seok, primary, Kim, Hyun Joon, additional, Goo, Bo Mee, additional, Park, Hyo Jin, additional, Kim, Choong Won, additional, Chung, Ky Hyun, additional, Park, Hyung Chul, additional, Chang, Se-Ho, additional, Kim, Yeon Woong, additional, Kim, Deok Ryong, additional, Cho, Gyeong Jae, additional, Choi, Wan Sung, additional, and Kang, Kee Ryeon, additional

Published
2006
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19. Oxidative Stress-dependent Structural and Functional Switching of a Human 2-Cys Peroxiredoxin Isotype II That Enhances HeLa Cell Resistance to H2O2-induced Cell Death

Author

Moon, Jeong Chan, primary, Hah, Young-Sool, additional, Kim, Woe Yeon, additional, Jung, Bae Gyo, additional, Jang, Ho Hee, additional, Lee, Jung Ro, additional, Kim, Sun Young, additional, Lee, Young Mee, additional, Jeon, Min Gyu, additional, Kim, Choong Won, additional, Cho, Moo Je, additional, and Lee, Sang Yeol, additional

Published
2005
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31. Cytosolic accumulation of ?H2AX is associated with tropomyosin-related kinase A-induced cell death in U2OS cells

Author

Jung, Eun Joo, Kim, Choong Won, and Kim, Deok Ryong

Abstract

Tropomyosin-related kinase A (TrkA) plays an important role in cell survival, differentiation, and apoptosis in various neuronal and nonneuronal cell types. Here we show that TrkA overexpression by the Tet-On system mimics NGF-mediated activation pathways in the absence of nerve growth factor (NGF) stimulation in U2OS cells. In addition, p53 upregulation upon DNA damage was inhibited by TrkA, and p21 was upregulated by TrkA in a p53-independent manner. TrkA overexpression caused cell death by interrupting cell cycle progression, and TrkA-induced cell death was diminished in the presence of its specific inhibitor GW441756. Interestingly, TrkA-mediated cell death was strongly related to ?H2AX production and poly (ADP-ribose) polymerase cleavage in the absence of DNA damage inducer. In this study, we also reveal that ?H2AX production by TrkA is blocked by TrkA kinase inhibitors K-252a and GW441756, and it is also significantly inhibited by JNK inhibitor SP600125. Moreover, reduction of cell viability by TrkA was strongly suppressed by SP600125 treatment, suggesting a critical role of JNK in TrkA-induced cell death. We also found that ?H2AX and TrkA were colocalized in cytosol in the absence of DNA damage, and the nuclear localization of ?H2AX induced by DNA damage was partly altered to cytosol by TrkA overexpression. Our results suggest that the abnormal cytosolic accumulation of ?H2AX is implicated in TrkA-induced cell death in the absence of DNA damage.

Published
2008
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32. Multiple Phosphorylation of Chicken Protein Tyrosine Phosphatase 1 and Human Protein Tyrosine Phosphatase 1B by Casein Kinase II and p60c-srcin Vitro

Author

Jung, Eun Joo, Kang, Yoon-Se, and Kim, Choong Won

Abstract

We have cloned a soluble chicken protein tyrosine phosphatase, named CPTP1, from the cDNA library of chicken intestine. The CPTP1 showed 92% sequence identity to the corresponding 321 amino acid residues of human PTP1B (HPTP1B). CPTP1 lacked 13 amino acids of the N-terminal region compared with HPTP1B, while the C-terminal 48 amino acid sequence of this protein was distinct from those of other PTPs.In vitrophosphorylation and phosphoamino acid analysis showed that both CPTP1 and HPTP1B were phosphorylated on serine and threonine residues near their N-terminus by casein kinase II (CKII). Furthermore, phosphorylation of CPTP1 by CKII resulted in an inhibition of its phosphatase activityin vitro.Interestingly, both CPTP1 and HPTP1B were also tyrosine-phosphorylated near their N-terminus by p60c-src. When we examined the vanadate effect, in the absence of vanadate, the tyrosine-phosphorylated CPTP1 by p60c-srcwas autodephosphorylated by its own phosphatase activity. These results suggest that both CPTP1 and HPTP1B might play an important role in CKII- and p60c-src-induced signal transduction cascades.

Published
1998
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33. Cytosolic accumulation of gammaH2AX is associated with tropomyosin-related kinase A-induced cell death in U2OS cells.

Author

Jung EJ, Kim CW, and Kim DR

Subjects
Anthracenes pharmacology, Apoptosis drug effects, Carbazoles pharmacology, Cell Cycle drug effects, Cell Cycle genetics, Cell Line, Tumor, Cyclin-Dependent Kinase Inhibitor p21 genetics, Cytosol drug effects, Cytosol enzymology, Cytosol ultrastructure, DNA Damage drug effects, DNA Damage genetics, Doxorubicin pharmacology, Humans, Indole Alkaloids pharmacology, MAP Kinase Kinase 4 antagonists & inhibitors, Nerve Growth Factor antagonists & inhibitors, Nerve Growth Factor metabolism, Phosphorylation drug effects, Protein Binding, Receptor, trkA antagonists & inhibitors, Receptor, trkA metabolism, Signal Transduction, Transfection, Apoptosis genetics, Cyclin-Dependent Kinase Inhibitor p21 biosynthesis, Histones metabolism, Protein Transport drug effects, Protein Transport genetics, Receptor, trkA genetics
Abstract

Tropomyosin-related kinase A (TrkA) plays an important role in cell survival, differentiation, and apoptosis in various neuronal and nonneuronal cell types. Here we show that TrkA overexpression by the Tet-On system mimics NGF-mediated activation pathways in the absence of nerve growth factor (NGF) stimulation in U2OS cells. In addition, p53 upregulation upon DNA damage was inhibited by TrkA, and p21 was upregulated by TrkA in a p53-independent manner. TrkA overexpression caused cell death by interrupting cell cycle progression, and TrkA-induced cell death was diminished in the presence of its specific inhibitor GW441756. Interestingly, TrkA-mediated cell death was strongly related to gammaH2AX production and poly (ADP-ribose) polymerase cleavage in the absence of DNA damage inducer. In this study, we also reveal that gammaH2AX production by TrkA is blocked by TrkA kinase inhibitors K-252a and GW441756, and it is also significantly inhibited by JNK inhibitor SP600125. Moreover, reduction of cell viability by TrkA was strongly suppressed by SP600125 treatment, suggesting a critical role of JNK in TrkA-induced cell death. We also found that gammaH2AX and TrkA were colocalized in cytosol in the absence of DNA damage, and the nuclear localization of gammaH2AX induced by DNA damage was partly altered to cytosol by TrkA overexpression. Our results suggest that the abnormal cytosolic accumulation of gammaH2AX is implicated in TrkA-induced cell death in the absence of DNA damage.

Published
2008
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