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Lipopolysaccharide-mediated protein expression profiling on neuronal differentiated SH-SY5Y cells

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dc.contributor.authorDas, Nando Dulal-
dc.contributor.authorChoi, Mi Ran-
dc.contributor.authorJung, Kyoung Hwa-
dc.contributor.authorPark, Ji Hyun-
dc.contributor.authorLee, Hyung Tae-
dc.contributor.authorKim, Seung Hyun-
dc.contributor.authorChai, Young Gyu-
dc.date.accessioned2022-07-16T15:15:01Z-
dc.date.available2022-07-16T15:15:01Z-
dc.date.issued2012-06-
dc.identifier.issn1976-0280-
dc.identifier.issn2092-7843-
dc.identifier.urihttps://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/165476-
dc.description.abstractNeuroinflammation can contribute to neuronal dysfunction, death and several neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and multiple sclerosis. Lipopolysaccharide (LPS)-induced neuroinflammation severely affects neurons and can contribute to neuronal dysfunction and degeneration by causing the release of inflammatory and neurotoxic factors. We evaluated the long-term effects of treating differentiated SH-SY5Y cells with LPS to mimic LPS-induced neuroinflammation. Using matrix assisted laser desorption ionization-time of flight mass spectrometry and MetaCore pathway analysis software (GeneGo), the proteomic expression profiles of differentiated SH-SY 5Y cells after LPS treatment was studied to determine the inflammatory effects on the process of SH-SY5Y differentiation. Long-term LPS treatment resulted in the upregulation of phosphodiesterase 4B (PDE4B), slit robo GTPase (SRGAP2), transcription repressor E2F-6, vimentin, and 70 kDa heat shock protein 9 (Mortalin/HSPA9). Taken together, our results suggest that LPS-treated differentiation of SH-SY5Y cells can lend insight into the multiple pathways involved in neurological diseases.-
dc.format.extent9-
dc.language영어-
dc.language.isoENG-
dc.publisher한국바이오칩학회-
dc.titleLipopolysaccharide-mediated protein expression profiling on neuronal differentiated SH-SY5Y cells-
dc.typeArticle-
dc.publisher.location대한민국-
dc.identifier.doi10.1007/s13206-012-6209-1-
dc.identifier.scopusid2-s2.0-84862575426-
dc.identifier.wosid000305404500009-
dc.identifier.bibliographicCitationBioChip Journal, v.6, no.2, pp 165 - 173-
dc.citation.titleBioChip Journal-
dc.citation.volume6-
dc.citation.number2-
dc.citation.startPage165-
dc.citation.endPage173-
dc.type.docTypeArticle-
dc.identifier.kciidART001668204-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.description.journalRegisteredClasskciCandi-
dc.relation.journalResearchAreaBiochemistry & Molecular Biology-
dc.relation.journalResearchAreaChemistry-
dc.relation.journalResearchAreaScience & Technology - Other Topics-
dc.relation.journalWebOfScienceCategoryBiochemical Research Methods-
dc.relation.journalWebOfScienceCategoryChemistry, Analytical-
dc.relation.journalWebOfScienceCategoryNanoscience & Nanotechnology-
dc.subject.keywordPlusHUMAN NEUROBLASTOMA-CELLS-
dc.subject.keywordPlusRETINOIC ACID-
dc.subject.keywordPlusBLASTOMA CELLS-
dc.subject.keywordPlusGROWTH-
dc.subject.keywordPlusACTIVATION-
dc.subject.keywordPlusMORTALIN-
dc.subject.keywordPlusDISEASE-
dc.subject.keywordPlusCULTURE-
dc.subject.keywordAuthorSH-SY5Y cells-
dc.subject.keywordAuthorLipopolysaccharide-
dc.subject.keywordAuthorMetaCore pathway analysis software (GeneGo)-
dc.subject.keywordAuthorNeuroinflammation-
dc.identifier.urlhttps://link.springer.com/article/10.1007/s13206-012-6209-1-
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