Genome-wide evidences of bisphenol a toxicity using Schizosaccharomyces pombe
DC Field | Value | Language |
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dc.contributor.author | Kim, Dong-Myung | - |
dc.contributor.author | Heo, Jeonghoon | - |
dc.contributor.author | Lee, Dong Woo | - |
dc.contributor.author | Tsuji, Mayumi | - |
dc.contributor.author | Yang, Mihi | - |
dc.date.available | 2021-02-22T08:46:05Z | - |
dc.date.issued | 2018-08 | - |
dc.identifier.issn | 0253-6269 | - |
dc.identifier.issn | 1976-3786 | - |
dc.identifier.uri | https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/4395 | - |
dc.description.abstract | To clarify reliable toxic mechanisms of bisphenol A (BPA), an endocrine disrupting chemical, we approached an alternative animal and whole genome analyses with the yeast knockout library (YKO) of Schizosaccharomyces pombe. As results, the 50% growth inhibition concentrations (GI(50)) of BPA was approximately 600 mu M and the YKO-three step screening revealed the top 10 target candidate genes including dbp2, utp18, srs1, tif224, use1, qcr1, etc. The screening results were confirmed in human embryonic stem cell (hES)-derived hepatic cells and HepG2 human liver cancer cells. We found BPA down-regulated UQCRC, the human orthlog of S. pombe- qcr1, as a part of the mitochondrial respiratory chain, in HepG2 cells and hESs during cell differentiation into hepatic cells. Therefore, BPA may induce mitochondrial dysfunction and disruption of differentiation by suppressing UQCRC1. | - |
dc.format.extent | 8 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | PHARMACEUTICAL SOC KOREA | - |
dc.title | Genome-wide evidences of bisphenol a toxicity using Schizosaccharomyces pombe | - |
dc.type | Article | - |
dc.publisher.location | 대한민국 | - |
dc.identifier.doi | 10.1007/s12272-018-1058-7 | - |
dc.identifier.scopusid | 2-s2.0-85051839717 | - |
dc.identifier.wosid | 000443448800005 | - |
dc.identifier.bibliographicCitation | ARCHIVES OF PHARMACAL RESEARCH, v.41, no.8, pp 830 - 837 | - |
dc.citation.title | ARCHIVES OF PHARMACAL RESEARCH | - |
dc.citation.volume | 41 | - |
dc.citation.number | 8 | - |
dc.citation.startPage | 830 | - |
dc.citation.endPage | 837 | - |
dc.type.docType | Article | - |
dc.identifier.kciid | ART002378149 | - |
dc.description.isOpenAccess | N | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.description.journalRegisteredClass | kci | - |
dc.relation.journalResearchArea | Pharmacology & Pharmacy | - |
dc.relation.journalWebOfScienceCategory | Chemistry, Medicinal | - |
dc.relation.journalWebOfScienceCategory | Pharmacology & Pharmacy | - |
dc.subject.keywordPlus | MITOCHONDRIAL DYSFUNCTION | - |
dc.subject.keywordPlus | OXIDATIVE STRESS | - |
dc.subject.keywordPlus | SMALL MOLECULES | - |
dc.subject.keywordPlus | FISSION YEAST | - |
dc.subject.keywordPlus | CELLS | - |
dc.subject.keywordPlus | EXPOSURE | - |
dc.subject.keywordPlus | IDENTIFICATION | - |
dc.subject.keywordPlus | PROLIFERATION | - |
dc.subject.keywordPlus | HEPATOCYTES | - |
dc.subject.keywordPlus | INHIBITION | - |
dc.subject.keywordAuthor | Bisphenol A | - |
dc.subject.keywordAuthor | Differentiation | - |
dc.subject.keywordAuthor | UQCRC1 | - |
dc.subject.keywordAuthor | Genome | - |
dc.subject.keywordAuthor | Mitochondria | - |
dc.subject.keywordAuthor | Yeast | - |
dc.identifier.url | https://link.springer.com/article/10.1007/s12272-018-1058-7 | - |
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