Project description:This SuperSeries is composed of the following subset Series:; GSE11550: Hs 294T Cells Treated with Elesclomol Alone or in Combination with Paclitaxel Compared to DMSO Treated; GSE11551: Hs 294T Cells Treated with Elesclomol Alone or in Combination with NAC Compared to DMSO Treated Experiment Overall Design: Refer to individual Series
Project description:We used microarrays to detail gene expression changes in Hs 294T human melanoma cells after treatment with elesclomol alone, or in combination with NAC, to aide in identifing the mechnism of action of elesclomol. Experiment Overall Design: Hs 294T human melanoma cells were grown in vitro. They were seeded at a low density and were left untreated, treated with the vehicle, treated with elesclomol, treated with NAC, or treated in combination with both elesclomol and NAC. The cells treated with NAC were given the NAC 30 minutes prior to additional treatments. They were incubated for 6 hours before harvesting.
Project description:We used microarrays to detail gene expression changes in Hs 294T human melanoma cells after treatment with elesclomol alone, or in combination with NAC, to aide in identifing the mechnism of action of elesclomol. Keywords: treatment
2008-05-29 | GSE11551 | GEO
Project description:Hs 294T Cells Treated with Elesclomol in Combination with Paclitaxel or NAC
Project description:We used microarrays to detail gene expression changes in Hs 294T human melanoma cells after treatment with elesclomol alone, or in combination with paclitaxel, to aide in identifing the mechnism of action of elesclomol. Experiment Overall Design: Hs 294T human melanoma cells were grown in vitro. They were seeded at a low density and were left untreated, treated with the vehicle, treated with elesclomol, treated with paclitaxel, or treated in combination with both elesclomol and paclitaxel. They were incubated for 6 hours before harvesting.
Project description:To investigate the mechanisms by which SYK inhibition sensitizes OCI-mIDH1/N cells to ivosidenib, we performed RNA sequencing (RNA-seq) analysis of cells treated with DMSO (vehicle control), ivosidenib alone, fostamatinib alone, entospletinib alone, or the combination of ivosidenib with each of the two SYK inhibitors for 9 days.
Project description:We treated HEK293 cells with the cardiotonic steroid digitoxin to identify alternative splicing changes as compared to DMSO treatment alone.
Project description:Infiltration of peripheral immune cells after blood-brain barrier (BBB) dysfunction causes severe inflammation after a stroke. Although the endothelial glycocalyx functions as a barrier to circulating cells, the relationship between stroke severity and glycocalyx dysfunction remains unclear. In this study, glycosaminoglycans (GAGs), a component of the endothelial glycocalyx, in ischemic stroke were studied using a photochemically induced thrombosis (PIT) mouse model. As results, decreased levels of heparan sulfate (HS) and chondroitin sulfate (CS) and increased activity of hyaluronidase 1 and heparanase (HPSE) were observed in ischemic brain tissues. HPSE expression in cerebral vessels increased after stroke onset and infarct volume greatly decreased after co-administration of N-acetylcysteine (NAC)+GAG oligosaccharides as compared to NAC administration alone. These results suggest that the endothelial glycocalyx was injured after the onset of stroke. Interestingly, scission activity of proHPSE produced by HBMEC/ciβ and HEK293 cells transfected with hHPSE1 cDNA were activated by acrolein exposure. We identified the ACR modified amino acid residues of proHPSE using nano LC-MS/MS, suggesting that ACR modification of Lys139 (6-kDa linker), and Lys107 and Lys161, located in the immediate vicinity of the 6-kDa linker, at least in part, is attributed to the activation of proHPSE. Since proHPSE, but not HPSE, localizes outside cells by binding with HS proteoglycans, ACR-modified proHPSE represents a promising target to protect the endothelial glycocalyx.
Project description:Our goal is to investigate the effects of CD44 knockdown alone and in combination with Temozolomide on glioblastoma multiforme cells. To achieve this, we treated U251 cells that had been transfected with either shCtrl lentivirus or shCD44 lentivirus with either DMSO or Temozolomide.
