Project description:microRNA profiling of comparing control or ETO2 siRNA-treated human K562 cells Two-condition experiment, K562-control siRNA vs. K562-ETO2 siRNA, Biological replicates: 1, 1 control siRNA, 1 ETO2 siRNA, independently.
Project description:microRNA profiling of human K562 cells comparing control or ETO2-overexpressed cells Two-condition experiment, K562-pcDNA vs. K562-pcDNA-ETO2, Biological replicates: 1, 1 pcDNA, 1 pcDNA-ETO2, independently.
Project description:Transcriptional profiling of human hTERT-RPE1 cell spheroids comparing Control siRNA transfected hTERT-RPE1 cell spheroids with those transfected with YAP1 siRNA.
Project description:We used microarrays to examine what genes could be regulated by ETO2 in erythroid cells. Comparing expression profile in murine G1E-ER-GATA-1 cells treated with control and ETO2(Cbfa2t3) siRNA on Agilent array. After siRNA transfection, the cells were treated with b-estradiol for 24h to induce GATA-1-mediated erythroid maturation.
Project description:Transcriptional profiling of human hTERT-RPE1 cell spheroids comparing Control siRNA transfected hTERT-RPE1 cell spheroids with those transfected with YAP1 siRNA. Two-condition experiment, Control siRNA vs.YAP1 siRNA hTERT-RPE1 cell spheroids. Biological replicates: 1 Control siRNA, 1YAP1 siRNA transfected, independently grown and harvested. Bothreplicates per array.
Project description:Erythroid cell lines (HEL and K562) were conditionally invalidated for the ETO2 gene using the CRISPR/Cas9 system. Gene expression profiling (RNAseq) and chromatin immunoprecipitation followed by high-throughput sequencing (ChIPseq) to assess localization of ETO2, MYB, EP300, H3K27ac and H3K4me3 was performed in control and ETO2-deficient cells. ChIPseq analyses were also performed on cells from human AEL patient-derived xenograft models.
Project description:Comparing the transcriptomic profiles of GBM-37 cells treated with control and NUPR1 v.1 siRNA. Goal was to examine the effects of NUPR1 v.1 on malignant mesenchymal transformation of GBM tumor after conventional treatment