Eun Young Park

Gwangju Institute of Science and Technology, Gwangju, Gwangju, South Korea

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Publications (187)395.8 Total impact

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    ABSTRACT: In angiogenesis, circulating mononuclear cells are recruited to vascular lesions; however, the underlying mechanisms are poorly understood. Here, we characterize the functional role of protein tyrosine kinase 7 (PTK7)-expressing CD11b(+) mononuclear cells in vitro and in vivo using a mouse model of angiogenesis. Although the frequencies of PTK7(+)CD11b(+) cells in the bone marrow remained similar after vascular endothelial growth factor-A-induced neovascularization, we observed an 11-fold increase in the cornea. Importantly, vascular endothelial growth factor-A-induced chemotaxis of PTK7(+) cells was mediated by vascular endothelial growth factor receptor 2. In a coculture with endothelial cells, PTK7(+)CD11b(+) cells stabilized the vascular network for 2 weeks by expressing high levels of angiopoietin-1. The enhanced vascular stability was abolished by knockdown of angiopoietin-1 in PTK7(+)CD11b(+) cells and could be restored by angiopoietin-1 treatment. We conclude that PTK7 expression in perivascular mononuclear cells induces vascular endothelial growth factor receptor 2 and angiopoietin-1 expression and thus contributes to vascular stabilization in angiogenesis. © 2015 American Heart Association, Inc.
    Arteriosclerosis Thrombosis and Vascular Biology 05/2015; DOI:10.1161/ATVBAHA.114.305228 · 5.53 Impact Factor
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    ABSTRACT: Autosomal polycystic kidney disease (ADPKD) is a highly prevalent genetic renal disorder in which epithelial-lining fluid-filled cysts appear in kidneys. It is accompanied by hyperactivation of cell proliferation, interstitial inflammation, and fibrosis around the cyst lining cells, finally reaching end-stage renal disease. Previously, we found high expression of ligands stimulating the receptor for advanced glycation end products (RAGE) in ADPKD mice. Furthermore, gene silencing of RAGE was revealed to cause reduction of cystogenesis via down-regulation of cell proliferation in vitro, and intravenous administration of anti-RAGE adenovirus in vivo also displayed alleviation of the disease. Here, we attempted to identify the role of soluble RAGE (sRAGE) in inhibiting the progression of ADPKD using 2 different ADPKD mice models. sRAGE is an endogenously expressed form of RAGE that has no membrane-anchoring domain, thereby giving it the ability to neutralize the ligands that stimulate RAGE signals. Both overexpression of sRAGE and sRAGE treatment blocked RAGE-mediated cell proliferation in vitro. In addition, sRAGE-injected ADPKD mice showed reduced cysts accompanied by enhanced renal function, inhibition of cell proliferation, inflammation, and fibrosis. These positive therapeutic effects of sRAGE displayed little liver toxicity, suggesting it as a new potential therapeutic target of ADPKD with low side effects.-Lee, E. J., Park, E. Y., Mun, H., Chang, E., Ko, J. Y., Kim, D. Y., Park, J. H. Soluble receptor for advanced glycation end products inhibits disease progression in autosomal dominant polycystic kidney disease by down-regulating cell proliferation. © FASEB.
    The FASEB Journal 05/2015; DOI:10.1096/fj.15-272302 · 5.48 Impact Factor
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    ABSTRACT: In some countries with high smoking prevalence, smoke-free legislation has only been implemented in specific public places, as opposed to a comprehensive ban on smoking in all public places. The purpose of this study was to provide valid data on SHS exposure that reflect the consequences of incomplete smoke-free legislation, and provide a rationale for expanding this legislation. Indoor and outdoor environmental exposure (PM2.5, air nicotine, and dust NNK) was monitored in 35 public places where smoking is prohibited by law in Goyang, Republic of Korea. Biomarkers of SHS exposure (urinary cotinine, hair nicotine, and urinary NNAL) were measured in 37 non-smoking employees. Geometric means and standard deviations were used in comparison of each measure. Considerable exposure of SHS was detected at all indoor monitoring sites (PM2.5: 95.5 μg/m3 in private educational institutions, air nicotine: 0.77 μg/m3 in large buildings, and dust NNK: 160.3 pg/mg in large buildings); environmental measures were higher in private or closed locations, such as restrooms. Outdoor measures of SHS exposure were lowest in nurseries and highest in government buildings. Biochemical measures revealed a pattern of SHS exposure by monitoring site, and were highest in private educational institutions. The evidence of SHS exposure in legislative smoke free places in Korea suggests that incomplete smoke free legislation and lack of enforcement of it might not protect people from exposure to smoke. Therefore, active steps should be taken toward a comprehensive ban on smoking in all public places and its enforcement.
    Cancer Research and Treatment 04/2015; DOI:10.4143/crt.2014.269 · 2.98 Impact Factor
  • Cereal Chemistry 04/2015; DOI:10.1094/CCHEM-01-15-0007-R · 1.06 Impact Factor
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    ABSTRACT: To investigate the role of α3 and α7 nicotinic acetylcholine receptor subunits (nAChRs) in the bladder, using a rat model with detrusor overactivity induced by partial bladder outlet obstruction (BOO). Forty Sprague-Dawley rats were used: 10 were sham-operated (control group) and 30 were observed for 3 weeks after partial BOO. BOO-induced rats were further divided into 3 groups: Two groups of 10 rats each received intravesicular infusions with hexamethonium (HM group; n=10) or methyllycaconitine (MLC group; n=10), which are antagonists for α3 and α7 nAChRs, respectively. The remaining BOO-induced rats received only saline infusion (BOO group; n=10). Based on the contraction interval measurements using cystometrogram, the contraction pressure and nonvoiding bladder contractions were compared between the control and the three BOO-induced groups. Immunofluorescent staining and Western blotting were used to analyze α3 and α7 nAChRs levels. The contraction interval of the MLC group was higher than that of the BOO group (P<0.05). Nonvoiding bladder contraction almost disappeared in the HM and MLC groups. Contraction pressure increased in the BOO group (P<0.05) compared with the control group and decreased in the HM and MLC groups compared with the BOO group (P<0.05). Immunofluorescence staining showed that the α3 nAChR signals increased in the urothelium, and the α7 nAChR signals increased in the urothelium and detrusor muscle of the BOO group compared with the control group. Western blot analysis showed that both α3 and α7 nAChR levels increased in the BOO group (P<0.05). Alpha3 and α7 nAChRs are associated with detrusor overactivity induced by BOO. Furthermore, nAChR antagonists could help in clinically improving detrusor overactivity.
    International neurourology journal 03/2015; 19(1):12-8. DOI:10.5213/inj.2015.19.1.12
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    ABSTRACT: Mercury is a well-known environmental pollutant that can cause nephropathic diseases, including acute kidney injury (AKI). Although quercetin (QC), a natural flavonoid, has been reported to have medicinal properties, its potential protective effects against mercury-induced AKI have not been evaluated. In this study, the protective effect of QC against mercury-induced AKI was investigated using biochemical parameters, new protein-based urinary biomarkers, and a histopathological approach. A 250 mg/kg dose of QC was administered orally to Sprague-Dawley male rats for 3 days before administration of mercury chloride (HgCl2). All animals were sacrificed at 24 h after HgCl2 treatment, and biomarkers associated with nephrotoxicity were measured. Our data showed that QC absolutely prevented HgCl2-induced AKI, as indicated by biochemical parameters such as blood urea nitrogen (BUN) and serum creatinine (sCr). In particular, QC markedly decreased the accumulation of Hg in the kidney. Urinary excretion of protein-based biomarkers, including clusterin, kidney injury molecule-1 (KIM-1), neutrophil gelatinase-associated lipocalin (NGAL), monocyte chemoattractant protein-1 (MCP-1), tissue inhibitor of metalloproteinases 1 (TIMP-1), and vascular endothelial growth factor (VEGF) in response to HgCl2 administration were significantly decreased by QC pretreatment relative to that in the HgCl2-treated group. Furthermore, urinary excretion of metallothionein and Hg were significantly elevated by QC pretreatment. Histopathological examination indicated that QC protected against HgCl2-induced proximal tubular damage in the kidney. A TUNEL assay indicated that QC pretreatment significantly reduced apoptotic cell death in the kidney. The administration of QC provided significant protective effects against mercury-induced AKI.
    Journal of Medicinal Food 02/2015; 18(5). DOI:10.1089/jmf.2014.3242 · 1.70 Impact Factor
  • 01/2015; 10(1):61-63. DOI:10.17085/apm.2015.10.1.61
  • Cereal Chemistry 01/2015; 92(3):150121065624001. DOI:10.1094/CCHEM-09-14-0184-R · 1.06 Impact Factor
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    ABSTRACT: Transparent Pb(Zr,Ti)O3 (PZT) capacitors were fabricated using cost-effective solution process.•Photovoltaic response was investigated by introducing ultra-thin Pt layer between bottom electrode and PZT.•Introduction of Pt layer reduces the leakage current and enhances ferroelectric and PV response.•The transmittance of the capacitors were 45–50% in visible region.
    Solar Energy 01/2015; 111. DOI:10.1016/j.solener.2014.10.037 · 3.54 Impact Factor
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    Korean journal of anesthesiology 12/2014; 67(Suppl):S3-4. DOI:10.4097/kjae.2014.67.S.S3
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    ABSTRACT: The aim of this study was to investigate the effect of a 1.8-GHz continuous electromagnetic field (EMF) on wound healing in a human airway cell-culture system. In vitro study using a cell line. Immortalized human bronchial epithelial cells (a BEAS-2B cell line) were exposed to a 1.8-GHz EMF (specific absorption rate = 1.0 W/kg). We evaluated the effect of EMF on the cells using an 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyltetrazolium bromide (MTT) viability assay, by cell counting, and by using fluorescence-activated cell sorting (FACS) analysis of cell cycle dynamics and apoptosis. Inhibition of migration was tested by a wound-healing assay on scratched cell cultures. Cell migration in the wound-healing assay was decreased by the EMF treatment compared with controls. The MTT assay and cell counting consistently showed that the EMF used was not cytotoxic and did not inhibit cell proliferation. FACS analysis showed no alterations in the cell-cycle phase distribution or in apoptosis after EMF exposure. EMF can inhibit wound healing in vitro by inhibiting cell migration. N/A. Laryngoscope, 2014. © 2014 The American Laryngological, Rhinological and Otological Society, Inc.
    The Laryngoscope 12/2014; DOI:10.1002/lary.25109 · 2.03 Impact Factor
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    ABSTRACT: Human breast cancers include cancer stem cell populations as well as non-tumorigenic cancer cells. Breast cancer stem cells have self-renewal capability and are resistant to conventional chemotherapy. MicroRNAs (miRNAs) regulate the expression of many target genes; therefore, dysregulation of miRNAs have been associated with the pathogenesis of human diseases, including cancer. However, a role for miRNA dysregulation in stemness and drug resistance has yet to be identified. Members of the miR-34 family are reportedly tumor-suppressor miRNAs and are associated with various human cancers. Our results confirm that miR-34a expression was downregulated in MCF7/ADR cells compared with MCF7 cells. We hypothesized that this reduction was due to the p53 (TP53) mutation in MCF7/ADR cells. In this study, we found that primary and mature miR-34a were suppressed by treatment with p53 RNAi or the dominant negative p53 mutant in MCF7 cells. Ectopic miR-34a expression reduced cancer stem cell properties and increased sensitivity to doxorubicin treatment, by directly targeting NOTCH1. Furthermore, tumors from nude mice treated with miR-34a were significantly smaller compared to those of mice treated with control lentivirus. Our research suggests that the ectopic expression of miR-34a represents a novel therapeutic approach in chemoresistant breast cancer treatment.
    Cancer Research 11/2014; 74(24). DOI:10.1158/0008-5472.CAN-14-1140 · 9.28 Impact Factor
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    ABSTRACT: In nature, there exist a wide repertoire of dsRNA-binding proteins that have different binding modes for siRNA as well as structural differences, and some of these proteins have the potential as the effective siRNA delivery carriers. For delivering siRNA into cancer cells, a dsRNA-binding 2b protein derived from Tomato aspermy virus was genetically modified by fusing the integrin-targeting RGD peptide to its C-terminus, and biosynthesized. The resulting 2b-RGD protein possesses distinct characteristics favorable to biomedical applications of siRNA: (1) high affinity for siRNA, (2) siRNA protection against RNases in serum, (3) low cytotoxicity compared to the polycationic polymers often employed in the conventional siRNA carriers, (4) specific binding to integrins on cancer cells, and passing through the cell membrane via endocytosis, (5) ability to facilitate cytosolic release of siRNA. Here, we demonstrate the 2b-RGD/siRNA complexes have the high potential as a tumor-targeting siRNA delivery carrier and suggest their possible therapeutic applications for cancer treatment.
    Acta Biomaterialia 11/2014; 10(11). DOI:10.1016/j.actbio.2014.07.014 · 5.68 Impact Factor
  • Eun Young Park, Yoo Im Choi
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    ABSTRACT: [Purpose] The purpose of this study was to investigate the psychometric properties of the lower extremity subscale of the Fugl-Meyer Assessment lower extremity (FMA-LE) for community-dwelling hemiplegic stroke patients. [Subjects] The participants were 140 community-dwelling hemiplegic stroke patients. [Methods] To determine the psychometric properties of the FMA-LE, we examined construct validity, response characteristics, item discrimination, and internal consistency. [Results] Factor analysis of the FMA-LE revealed that the first factor explained 61.73% of the variance and provided evidence of unidimensionality. The FMA-LE did not show ceiling or floor effects; Cronbach's α was 0.935 (95% CI: 0.919-0.950). [Conclusion] Because the FMA-LE seems to be both valid and reliable, we conclude that it is appropriate for the measurement of the lower extremity motor impairment of community-dwelling hemiplegic stroke patients.
    Journal of Physical Therapy Science 11/2014; 26(11):1775-1777. DOI:10.1589/jpts.26.1775 · 0.20 Impact Factor
  • Eun Young Park, Eun-Nam Lee
    10/2014; 26(5):500-511. DOI:10.7475/kjan.2014.26.5.500
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    ABSTRACT: Previously, we showed that retinol (vitamin A) decreased both colorectal cancer cell invasion and phosphatidylinositol 3-kinase (PI3K) activity through a retinoic acid receptor-independent mechanism. Here, we determined if these phenomena were related by using parental HCT-116 cells that harbor 1 allele of wild-type PI3K and 1 allele of constitutively active (ca) PI3K and 2 mutant HCT-116 cell lines homozygous for caPI3K. In vitro, treatment of parental HCT-116 cells with 10 μM retinol reduced cell invasion whereas treatment of mutant HCT-116 cell lines with retinol did not. Treatment with 10 μM retinol also decreased the activity of matrixmetalloproteinase-9 and increased tissue inhibitor of matrixmetalloproteinase-I levels in parental, but not mutant, HCT-116 cells. Finally, parental or mutant cells were intrasplenically injected into athymic mice consuming diets with or without supplemental vitamin A. As expected, vitamin A supplementation tended (P = 0.18) to reduce the incidence of metastases in mice injected with the parental cell line and consuming the supplemented diet. In contrast, metastatic incidence was not affected (P = 1.00) by vitamin A supplementation in mice injected with mutant cells. These data indicate that the capacity of retinol to inhibit PI3K activity confers its ability to decrease colorectal cancer metastasis.
    Nutrition and Cancer 10/2014; 66(8):1-10. DOI:10.1080/01635581.2014.956258 · 2.47 Impact Factor
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    ABSTRACT: The aim of this study was to investigate urinary metabolomic profiles associated with cadmium (Cd)-induced nephrotoxicity and their potential mechanisms. Metabolomic profiles were measured by high-resolution (1)H-nuclear magnetic resonance (NMR) spectroscopy in the urine of rats after oral exposure to CdCl2 (1, 5, or 25 mg/kg) for 6 wk. The spectral data were further analyzed by a multivariate analysis to identify specific urinary metabolites. Urinary excretion levels of protein biomarkers were also measured and CdCl2 accumulated dose-dependently in the kidney. High-dose (25 mg/kg) CdCl2 exposure significantly increased serum blood urea nitrogen (BUN), but serum creatinine (sCr) levels were unchanged. High-dose CdCl2 (25 mg/kg) exposure also significantly elevated protein-based urinary biomarkers including osteopontin, monocyte chemoattractant protein-1 (MCP-1), kidney injury molecules-1 (Kim-1), and selenium-binding protein 1 (SBP1) in rat urine. Under these conditions, six urinary metabolites (citrate, serine, 3-hydroxyisovalerate, 4-hydroxyphenyllactate, dimethylamine, and betaine) were involved in mitochondrial energy metabolism. In addition, a few number of amino acids such as glycine, glutamate, tyrosine, proline, or phenylalanine and carbohydrate (glucose) were altered in urine after CdCl2 exposure. In particular, the metabolites involved in the glutathione biosynthesis pathway, including cysteine, serine, methionine, and glutamate, were markedly decreased compared to the control. Thus, these metabolites are potential biomarkers for detection of Cd-induced nephrotoxicity. Our results further indicate that redox metabolomics pathways may be associated with Cd-mediated chronic kidney injury. These findings provide a biochemical pathway for better understanding of cellular mechanism underlying Cd-induced renal injury in humans.
    Journal of Toxicology and Environmental Health Part A 10/2014; 77(22-24):1384-98. DOI:10.1080/15287394.2014.951755 · 1.83 Impact Factor
  • Myungsun Yi, Keeho Park, Eun Young Park
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    ABSTRACT: The purpose of the study was to investigate significant psychosocial needs of low-income people with cancer in Korea and the extent to which these needs are unmet and which factors influence them.
    European journal of oncology nursing: the official journal of European Oncology Nursing Society 10/2014; 18(6). DOI:10.1016/j.ejon.2014.07.005 · 1.79 Impact Factor
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    ABSTRACT: Excessive reactive oxygen species (ROS) production plays a crucial role in causing various diseases, including inflammatory disorders. The activation of mitogen-activated protein kinase (MAPK) and nuclear factor-kappaB (NF-κB) signaling is implicated in stimulating inflammatory response and cytokines. Peroxiredoxin 2 (Prx2) is a 2-cysteine (Cys) peroxiredoxin capable of removing endogenous hydrogen peroxide (H2O2). PEP-1 peptide, a protein transduction domain, consists of three domains which are used to transduce exogenous therapeutic proteins into cells. The correlation between effectively transduced PEP-1-Prx2 and ROS-mediated inflammatory response is not clear. In the present study, we investigated the protective effects of cell permeable PEP-1-Prx2 on oxidative stress-induced inflammatory activity in Raw 264.7 cells and in a mouse ear edema model after exposure to lipopolysaccharides (LPS) or 12-O-tetradecanoylphorbol-13-actate (TPA). Transduced PEP-1-Prx2 suppressed intracellular ROS accumulation and inhibited the activity of MAPKs and NF-κB signaling that led to the suppression of cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS) and cytokines in LPS-induced Raw 264.7 cells and TPA-induced mouse ear edema model. Given these results, we propose that PEP-1-Prx2 has therapeutic potential in the prevention of inflammatory disorders.
    International Immunopharmacology 09/2014; 23(2). DOI:10.1016/j.intimp.2014.09.008 · 2.71 Impact Factor
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    Su Yeon Kye, Eun Young Park, Kyounghee Oh, Keeho Park
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    ABSTRACT: The aims of the present study were to assess the prevalence of perceived risk for cancer; to explore associations between sociodemographics and family history of cancer and perceived cancer risk; to identify perceived cause of cancer risk; and to examine the associations between sociodemographics and family history of cancer and perceived cause of cancer risk. This cross-sectional study was conducted among 1,009 participants aged 30-69 years, selected from a population-based database in October 2009 through multiple-stratified random sampling. Information was collected about the participants' perceived cancer risk and perceived cause of cancer risk. Overall, 59.5% of the respondents thought they had the chance of developing cancer. Female sex, younger age, lower income, and family history of cancer were positively associated with perceived cancer risk. The most important perceived cause of cancer risk was stress. There was a difference between sociodemographics and family history of cancer and perceived cause of cancer risk. Factors affecting perceptions of cancer risk and cause of cancer risk need to be addressed in risk communications. The results provide important directions for the development of educational strategies to promote awareness and self-appraisal of cancer risk and risk factors.
    Cancer Research and Treatment 09/2014; 47(2). DOI:10.4143/crt.2014.024 · 2.98 Impact Factor

Publication Stats

2k Citations
395.80 Total Impact Points

Institutions

  • 2015
    • Gwangju Institute of Science and Technology
      • School of Materials Science and Engineering
      Gwangju, Gwangju, South Korea
  • 2007–2015
    • Sookmyung Women's University
      • Department of Biological Science
      Sŏul, Seoul, South Korea
  • 2005–2015
    • Catholic University of Korea
      • • Department of Urology
      • • College of Medicine
      • • Department of Internal Medicine
      Sŏul, Seoul, South Korea
    • Seoul National University Hospital
      • Department of Nuclear Medicine
      Sŏul, Seoul, South Korea
  • 2014
    • Texas State University
      • School of Family and Consumer Sciences
      سان ماركوس، تكساس, Texas, United States
  • 2013–2014
    • Kyungpook National University
      • Green-Nano Materials Research Center
      Daikyū, Daegu, South Korea
    • Ajou University
      • Department of Otolaryngology
      Sŏul, Seoul, South Korea
  • 2012–2014
    • Hallym University Medical Center
      • Department of Anesthesiology and Pain Medicine
      Sŏul, Seoul, South Korea
    • Pusan National University
      • • Department of Pathology
      • • Department of Surgery
      Tsau-liang-hai, Busan, South Korea
    • Chungnam National University
      • Department of Horticultural Science
      Daiden, Daejeon, South Korea
    • Harvard University
      Cambridge, Massachusetts, United States
    • Korea Research Institute of Chemical Technology
      Daiden, Daejeon, South Korea
    • California State University, San Marcos
      San Marcos, California, United States
    • Harvard Medical School
      Boston, Massachusetts, United States
  • 2011–2014
    • Gachon University
      • • Department of Nursing (College of Nursing)
      • • Lee Gil Ya Cancer and Diabetes Institute
      Sŏngnam, Gyeonggi-do, South Korea
    • Jeonju University
      • Department of Secondary Special Education
      Sŏul, Seoul, South Korea
  • 2010–2014
    • Yonsei University
      Sŏul, Seoul, South Korea
    • University of Kentucky
      Lexington, Kentucky, United States
    • Korea Institute of Radiological & Medical Sciences
      Sŏul, Seoul, South Korea
  • 2004–2014
    • National Cancer Center Korea
      Kōyō, Gyeonggi Province, South Korea
  • 2011–2013
    • Hallym University
      • College of Medicine
      Sŏul, Seoul, South Korea
  • 2004–2013
    • Korea University
      • • College of Nursing
      • • Department of Life Sciences
      Sŏul, Seoul, South Korea
  • 2009–2011
    • Hannam University
      • Department of Advanced Materials
      Daiden, Daejeon, South Korea
  • 2004–2009
    • Ewha Womans University
      • • Department of Pediatrics
      • • Center for Cell Signaling Research (CCSR)
      Sŏul, Seoul, South Korea
  • 2008
    • Chonnam National University
      • Department of Pediatrics
      Gwangju, Gwangju, South Korea
    • Dong Seoul College
      Sŏul, Seoul, South Korea
  • 2007–2008
    • Hanyang University
      • Division of Chemical Engineering and Bioengineering
      Sŏul, Seoul, South Korea
  • 2005–2008
    • University of Texas at Austin
      • • Institute for Cellular and Molecular Biology
      • • School of Human Ecology
      Austin, Texas, United States
  • 2002–2008
    • Seoul National University
      • • Department of Preventive Medicine
      • • Research Institute of Pharmaceutical Sciences
      • • College of Pharmacy
      • • Department of Biological Sciences
      Sŏul, Seoul, South Korea
    • Hankuk University of Foreign Studies
      • Department of Bioscience and Biotechnology
      Sŏul, Seoul, South Korea
  • 2006
    • Molecular and Cellular Biology Program
      • Department of Microbiology and Institute for Cellular and Molecular Biology
      Seattle, Washington, United States
    • Kangbuk Samsung Hospital
      Sŏul, Seoul, South Korea