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dc.contributor.authorPark, Hye-Won-
dc.contributor.authorKim, Seung-Jun-
dc.contributor.authorAn, Yu Ri-
dc.contributor.authorKim, Jun-Sub-
dc.contributor.authorYu, So Yeon-
dc.contributor.authorOh, Moon-Ju-
dc.contributor.authorKim, Youn-Jung-
dc.contributor.authorRyu, Jae-Chun-
dc.contributor.authorHwang, Seung Yong-
dc.date.accessioned2024-01-20T19:33:39Z-
dc.date.available2024-01-20T19:33:39Z-
dc.date.created2021-09-02-
dc.date.issued2010-03-31-
dc.identifier.issn1738-642X-
dc.identifier.urihttps://pubs.kist.re.kr/handle/201004/131615-
dc.description.abstractThe endocrine system is a system of glands that secrete hormones to regulate the body. This system is disrupted by endocrine disrupting chemicals (EDCs), which are similar to sex hormones. These chemicals function as androgen antagonists or estrogen agonists. To determine the effect of EDCs on the gene expression profile in human cells, we treated HepG2 cells with 3 chemicals (bisphenol A, 17 beta-estradiol, vinclozolin), and analyzed common gene expression using a custom-made HazChem human array V3. The HazChem human array V3 included a total of 1136 genes, all of which were differentially expressed by exposure to VOCs, PAHs, POPs, and LTCs. Of these genes, 24 genes were commonly expressed after exposure to all 3 chemicals, based on the SAM (Significant Analysis of Microarray) method (q-value < 0.5%). These genes were analyzed further and found to be involved in coagulation, hemostasis, wound healing, angiogenesis, homeostasis, cell redox homeostasis, and cell proliferation based on GO function and pathway networks.-
dc.languageEnglish-
dc.publisherKOREAN SOCIETY TOXICOGENOMICS & TOXICOPROTEOMICS-KSTT-
dc.subjectTOXICITY-
dc.titleGene expression profiling of HepG2 cells treated with endocrine disrupting chemicals using the HazChem human array V3-
dc.typeArticle-
dc.identifier.doi10.1007/s13273-010-0008-3-
dc.description.journalClass1-
dc.identifier.bibliographicCitationMOLECULAR & CELLULAR TOXICOLOGY, v.6, no.1, pp.57 - 63-
dc.citation.titleMOLECULAR & CELLULAR TOXICOLOGY-
dc.citation.volume6-
dc.citation.number1-
dc.citation.startPage57-
dc.citation.endPage63-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.description.journalRegisteredClasskci-
dc.description.journalRegisteredClassother-
dc.identifier.kciidART001738040-
dc.identifier.wosid000276155300008-
dc.identifier.scopusid2-s2.0-77956761874-
dc.relation.journalWebOfScienceCategoryBiochemistry & Molecular Biology-
dc.relation.journalWebOfScienceCategoryToxicology-
dc.relation.journalResearchAreaBiochemistry & Molecular Biology-
dc.relation.journalResearchAreaToxicology-
dc.type.docTypeArticle-
dc.subject.keywordPlusTOXICITY-
dc.subject.keywordAuthorEDCs-
dc.subject.keywordAuthorHazChem-
dc.subject.keywordAuthorHepG2-
dc.subject.keywordAuthorBPA-
dc.subject.keywordAuthor17 beta-estradiol-
dc.subject.keywordAuthorVinclozolin-
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KIST Article > 2010
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