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14 results on '"Nam, Hyun-Ja"'

5. Spartan deficiency causes accumulation of Topoisomerase 1 cleavage complexes and tumorigenesis

Author

Maskey, Reeja S., primary, Flatten, Karen S., additional, Sieben, Cynthia J., additional, Peterson, Kevin L., additional, Baker, Darren J., additional, Nam, Hyun-Ja, additional, Kim, Myoung Shin, additional, Smyrk, Thomas C., additional, Kojima, Yusuke, additional, Machida, Yuka, additional, Santiago, Annyoceli, additional, van Deursen, Jan M., additional, Kaufmann, Scott H., additional, and Machida, Yuichi J., additional

Published
2017
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8. Parkin Regulates Mitosis and Genomic Stability through Cdc20/Cdh1

Author

Lee, Seung Baek, primary, Kim, Jung Jin, additional, Nam, Hyun-Ja, additional, Gao, Bowen, additional, Yin, Ping, additional, Qin, Bo, additional, Yi, Sang-Yeop, additional, Ham, Hyoungjun, additional, Evans, Debra, additional, Kim, Sun-Hyun, additional, Zhang, Jun, additional, Deng, Min, additional, Liu, Tongzheng, additional, Zhang, Haoxing, additional, Billadeau, Daniel D., additional, Wang, Liewei, additional, Giaime, Emilie, additional, Shen, Jie, additional, Pang, Yuan-Ping, additional, Jen, Jin, additional, van Deursen, Jan M., additional, and Lou, Zhenkun, additional

Published
2015
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10. Mitotic kinase cascades orchestrating timely disjunction and movement of centrosomes maintain chromosomal stability and prevent cancer.

Author

Ree, Janine, Nam, Hyun-Ja, and Deursen, Jan

Abstract

Centrosomes are microtubule-organizing centers that duplicate in S phase to form bipolar spindles that separate duplicated chromosomes faithfully into two daughter cells during cell division. Recent studies show that proper timing of centrosome dynamics, the disjunction and movement of centrosomes, is tightly linked to spindle symmetry, correct microtubule-kinetochore attachment, and chromosome segregation. Here, we review mechanisms that regulate centrosome dynamics, with emphasis on the roles of key mitotic kinases in the proper timing of centrosome dynamics and how aberrancies in these processes may cause chromosomal instability and cancer. [ABSTRACT FROM AUTHOR]

Published
2016
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13. Co-treatment with hepatocyte growth factor and TGF-ß1 enhances migration of HaCaT cells through NADPH oxidase-dependent ROS generation

Author

Nam, Hyun-Ja, Park, Yun-Yeon, Yoon, Gyesoon, Cho, Hyeseong, and Lee, Jae-Ho

Abstract

Wound healing requires re-epithelialization from the wound margin through keratinocyte proliferation and migration, and some growth factors are known to influence this process. In the present study, we found that the co-treatment with hapatocyte growth factor (HGF) and TGF-ß1 resulted in enhanced migration of HaCaT cells compared with either growth factor alone, and that N-acetylcysteine, an antioxidant agent, was the most effective among several inhibitors tested, suggesting the involvement of reactive oxygen species (ROS). Fluorescence-activated cell sorter analysis using 2',7'-dichlorofluorescein diacetate (DCF-DA) dye showed an early (30 min) as well as a late (24 h) increase of ROS after scratch, and the increase was more prominent with the growth factor treatment. Diphenyliodonium (DPI), a potent inhibitor of NADPH oxidase, abolished the increase of ROS at 30 min, followed by the inhibition of migration, but not the late time event. More precisely, gene knockdown by shRNA for either Nox-1 or Nox-4 isozyme of gp91phox subunit of NADPH oxidase abolished both the early time ROS production and migration. However, HaCaT cell migration was not enhanced by treatment with H2O2. Collectively, co-treatment with HGF and TGF-ß1 enhances keratinocyte migration, accompanied with ROS generation through NADPH oxidase, involving Nox-1 and Nox-4 isozymes.

Published
2010
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14. Co-treatment with hepatocyte growth factor and TGF-beta1 enhances migration of HaCaT cells through NADPH oxidase-dependent ROS generation.

Author

Nam HJ, Park YY, Yoon G, Cho H, and Lee JH

Subjects
Biphenyl Compounds pharmacology, Epithelium drug effects, Epithelium enzymology, Gene Knockdown Techniques, Humans, Hydrogen Peroxide pharmacology, Isoenzymes metabolism, Keratinocytes drug effects, NADPH Oxidase 1, NADPH Oxidase 4, Onium Compounds pharmacology, Phosphatidylinositol 3-Kinases metabolism, Protein Subunits metabolism, Signal Transduction drug effects, Time Factors, Cell Movement drug effects, Hepatocyte Growth Factor pharmacology, Keratinocytes cytology, Keratinocytes enzymology, NADPH Oxidases metabolism, Reactive Oxygen Species metabolism, Transforming Growth Factor beta1 pharmacology
Abstract

Wound healing requires re-epithelialization from the wound margin through keratinocyte proliferation and migration, and some growth factors are known to influence this process. In the present study, we found that the co-treatment with hepatocyte growth factor (HGF) and TGF-beta1 resulted in enhanced migration of HaCaT cells compared with either growth factor alone, and that N-acetylcysteine, an antioxidant agent, was the most effective among several inhibitors tested, suggesting the involvement of reactive oxygen species (ROS). Fluorescence-activated cell sorter analysis using 2,7-dichlorofluorescein diacetate (DCF-DA) dye showed an early (30 min) as well as a late (24 h) increase of ROS after scratch, and the increase was more prominent with the growth factor treatment. Diphenyliodonium (DPI), a potent inhibitor of NADPH oxidase, abolished the increase of ROS at 30 min, followed by the inhibition of migration, but not the late time event. More precisely, gene knockdown by shRNA for either Nox-1 or Nox-4 isozyme of gp91phox subunit of NADPH oxidase abolished both the early time ROS production and migration. However, HaCaT cell migration was not enhanced by treatment with H((2))O((2)). Collectively, co-treatment with HGF and TGF-beta1 enhances keratinocyte migration, accompanied with ROS generation through NADPH oxidase, involving Nox-1 and Nox-4 isozymes.

Published
2010
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