Young Rok Seo

ORCID: 0000-0002-4093-4073
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About
Contact & Profiles
Research Areas
  • Carcinogens and Genotoxicity Assessment
  • Heavy Metal Exposure and Toxicity
  • Selenium in Biological Systems
  • Air Quality and Health Impacts
  • Cancer-related Molecular Pathways
  • DNA Repair Mechanisms
  • Trace Elements in Health
  • Nanoparticles: synthesis and applications
  • Skin Protection and Aging
  • Glutathione Transferases and Polymorphisms
  • Genomics, phytochemicals, and oxidative stress
  • Chromium effects and bioremediation
  • Epigenetics and DNA Methylation
  • Effects and risks of endocrine disrupting chemicals
  • Genetics, Aging, and Longevity in Model Organisms
  • Molecular Biology Techniques and Applications
  • Air Quality Monitoring and Forecasting
  • Cancer Research and Treatments
  • Redox biology and oxidative stress
  • Invertebrate Immune Response Mechanisms
  • Microplastics and Plastic Pollution
  • Health, Environment, Cognitive Aging
  • Environmental Toxicology and Ecotoxicology
  • bioluminescence and chemiluminescence research
  • MicroRNA in disease regulation

Dongguk University
2015-2024

Rutgers, The State University of New Jersey
2024

Hospital General de Niños Ricardo Gutierrez
2024

Monash University
2024

Royal Manchester Children's Hospital
2024

University Hospital in Motol
2024

Bambino Gesù Children's Hospital
2024

IRCCS Materno Infantile Burlo Garofolo
2024

Mahidol University
2021

Jackson Laboratory
2018

Human cells lacking functional p53 exhibit a partial deficiency in nucleotide excision repair (NER), the pathway for of UV-induced DNA damage. The global genomic (GGR) subpathway NER, but not transcription-coupled (TCR), is mainly affected by loss or inactivation. We have utilized mouse embryo fibroblasts (MEFs) genes downstream effector pathway, gadd45 (Gadd45a) p21 (Cdkn1a), as well MEFs both and to address potential contribution these effectors p53-associated repair. Loss had pronounced...

10.1128/mcb.20.10.3705-3714.2000 article EN Molecular and Cellular Biology 2000-05-01

The cancer chemopreventive properties of selenium compounds are well documented, yet little is known the mechanism(s) by which these agents inhibit carcinogenesis. We show that in form selenomethionine (SeMet) can activate p53 tumor suppressor protein a redox mechanism requires factor Ref1. Assays to measure direct reduction/oxidation showed SeMet-dependent response was blocked dominant–negative By using peptide containing only cysteine residues 275 and 277, we demonstrate importance...

10.1073/pnas.212319799 article EN Proceedings of the National Academy of Sciences 2002-09-30

The capacity of DNA damaging agents to induce apoptosis is regulated by target gene induction p53. We found that p53 targeted MDM2 in cells which repair was occurring, but persistent damage induced chemotherapy led selectively PTEN. High dose the phosphorylation on serine 46, whereas low did not. A nonphosphorylatable 46 alanine mutant (S46A) promoter preference for aspartate (S46D, a mimic) PTEN MDM2. These observations show sufficient it (phosphatase and tensin homolog deleted chromosome...

10.1074/jbc.m503026200 article EN cc-by Journal of Biological Chemistry 2005-04-21

In this study, Bax inhibitor-1 (BI-1) overexpression reduces the ER pool of Ca2+ released by thapsigargin. Cells overexpressing BI-1 also showed lower intracellular release induced ionophore ionomycin as well agonists ryanodine receptors and inositol trisphosphate receptors. contrast, cells expressing carboxyl-terminal deleted (CΔ-BI-1 cells) displayed normal mobilization. Basal rates from were higher in BI-1-overexpressing than control or CΔ-BI-1 cells. We determined that cytosolic region...

10.1074/jbc.m800075200 article EN cc-by Journal of Biological Chemistry 2008-04-01

10.1007/s13530-018-0340-x article EN Toxicology and Environmental Health Sciences 2018-03-01

Nickel (Ⅱ) is a toxic and carcinogenic metal which induces redox imbalance following oxidative stress. Nuclear factor erythroid-2 related 2 (Nrf2) that regulates oxidation/reduction status consequently mediates cytoprotective responses against exposure to environmental toxicants. In this study, we investigated the protective roles of Nrf2 gene stress DNA damage induced by nickel at sub-lethal doses. Under conditions, detected significantly increased intracellular ROS generation, in addition...

10.3892/or.2012.2057 article EN cc-by-nc Oncology Reports 2012-09-26

This study determined the efficacy of carnosic acid (CA) for suppressing colon carcinogenesis associated with excess adiposity.Cell growth regulation by CA was evaluated in HT-29 adenocarcinoma cells cocultured 3T3-L1 adipocytes. To determine vivo efficacies, male A/J mice were divided into four groups and fed one following experimental diets 11 wk: 15% fat, 45% fat + 0.01% CA, or 0.02% CA. Azoxymethane administered at beginning diet two cycles dextran sodium sulfate supplied 1 wk after...

10.1002/mnfr.201400293 article EN Molecular Nutrition & Food Research 2014-09-09

Excess energy supply induces chronic low-grade inflammation in association with oxidative stress various tissues including intestinal epithelium. The objective of this study was to investigate the effect high-fat diet (HFD) on cell membrane integrity and tumorigenesis Apc(Min/+) mice.Mice were fed either normal (ND) or HFD for 12 weeks. number tumors counted biomarkers endotoxemia, stress, determined. Changes measured by fluorescein isothiocyanate (FITC)-dextran penetration gap junction...

10.15430/jcp.2016.21.2.95 article EN Journal of Cancer Prevention 2016-06-30

Background: Silver nanoparticles (AgNPs) are widely used in industrial and household applications, arousing concern regarding their safety humans. The risks posed by stabilizer-coated AgNPs continue to be unclear, assessing toxicity is for an understanding of the issues involved use various applications. Purpose: We aimed investigated long-term citrate-coated silver (cAgNPs) liver tissue using several tests transcriptomic analysis at 7 28 days after a single intravenous injection into rabbit...

10.2147/ijn.s174515 article EN cc-by-nc International Journal of Nanomedicine 2019-01-01
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