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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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ER stress impairs the insulin signaling pathway through mitochondrial damage in SH-SY5Y human neuroblastoma cells

ABSTRACT: This SuperSeries is composed of the following subset Series: GSE24497: ER stress impairs the insulin signaling pathway through mitochondrial damage in SH-SY5Y human neuroblastoma cells (part 1) GSE24499: ER stress impairs the insulin signaling pathway through mitochondrial damage in SH-SY5Y human neuroblastoma cells (part 2) Refer to individual Series

ORGANISM(S): Homo sapiens

SUBMITTER: hyun-jung koo

PROVIDER: E-GEOD-24500 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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ER stress impairs the insulin signaling pathway through mitochondrial damage in SH-SY5Y human neuroblastoma cells (part 2)

Project description:To investigate atrazine induced transcriptomes in SH-SY5Y cells Total RNA obtained from SH-SY5Y cells were treated with control vehicle (DMSO) or atrazine (ATZ).

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ER stress impairs the insulin signaling pathway through mitochondrial damage in SH-SY5Y human neuroblastoma cells (part 1)

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Project description:ER stress impairs the insulin signaling pathway through mitochondrial damage in SH-SY5Y human neuroblastoma cells

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Profiling neuroblastoma SH-SY5Y with Paraquat treatment

Project description:Human SH-SY5Y neuroblastoma cells treated with paraquat, a neurotoxic herbicide which both catalyzes the formation of reactive oxygen species (ROS) and induces mitochondrial damage in animal models was profiled using Affimetrix Exon 1.0 ST GeneChips® Human SH-SY5Y neuroblastoma cells was compared with respect to Human SH-SY5Y neuroblastoma cells treated with Paraquat. Parqaut treatment was done as described by Maracchioni, A., Totaro, A., Angelini, D.F., Di Penta, A., Bernardi, G., Carri, M.T., and Achsel, T. (2007) J Neurochem 100, 142-153

2010-12-22 | E-GEOD-21305 | biostudies-arrayexpress

Transcription profiling of human neuroblastoma SH-SY5Y cells: 4h identifies molecular effectors of unconjugated bilirubin

Project description:The deposition of unconjugated bilirubin (UCB) in selected regions of the brain results in irreversible neuronal damage, or Bilirubin Encephalopathy (BE). Although UCB impairs a large number of cellular functions, the basic mechanisms of neurotoxicity have not yet been fully clarified. While cells can accumulate UCB by passive diffusion, cell protection may involve multiple mechanisms including the extrusion of the pigment as well as pro-survival homeostatic responses that are still unknown. The effects of UCB treatment to SH-SY5Y neuroblastoma cell line were examined by high-density oligonucleotide microarrays. 230 genes were induced after 24 hours. A Gene Ontology (GO) analysis showed that a large group of UCB-induced genes were components of the ER stress response. Independent experimental validation of molecular events crucial for the ER stress response is presented. The results show that UCB exposure induces the ER stress response as a major intracellular homeostatic response in neuroblastoma cells in vitro. Our finding may provide valuable information for new therapeutic strategies in the treatment of BE. Experiment Overall Design: We used high-density oligonucleotide microarrays to analyze the gene expression profile of human neuroblastoma SH-SY5Y cells upon UCB treatment. Three replicates of UCB-treated cells were analyzed. As controls, we used three replicates of the same cells treated with DMSO only (the solvent used for UCB treatment).

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Transcription profiling of human neuroblatoma SH-SY5Y cells: 24h identifies molecular effectors of unconjugated bilirubin

Project description:The deposition of unconjugated bilirubin (UCB) in selected regions of the brain results in irreversible neuronal damage, or Bilirubin Encephalopathy (BE). Although UCB impairs a large number of cellular functions, the basic mechanisms of neurotoxicity have not yet been fully clarified. While cells can accumulate UCB by passive diffusion, cell protection may involve multiple mechanisms including the extrusion of the pigment as well as pro-survival homeostatic responses that are still unknown. The effects of UCB treatment to SH-SY5Y neuroblastoma cell line were examined by high density oligonucleotide microarrays. 230 genes were induced after 24 hours. A Gene Ontology (GO) analysis showed that a large group of UCB-induced genes were components of the ER stress response. Independent experimental validation of molecular events crucial for the ER stress response is presented. The results show that UCB exposure induces ER stress response as major intracellular homeostatic response in neuroblastoma cells in vitro. Our finding may provide valuable information for new therapeutic strategies in the treatment of BE. Experiment Overall Design: We used high density oligonucleotide microarrays to analyze the gene expression profile of human neuroblastoma SH-SY5Y cells upon UCB treatment. Three replicates of UCB-treated cells were analyzed. As controls, we used three replicates of the same cells treated with DMSO only (the solvent used for UCB treatment).

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