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: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.
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:Transcriptional profiling of HCT116 cells compared to untreated control with HCT116 cells transfected with ZNF746 siRNA plasmid. Goal was to determine the effects of ZNF746 gene transfection on CRC progression. Two-condition experiment, HCT116 vs. ZNF746 siRNA.
Project description:This series consists of samples taken from two groups of K562 cells(miR-181a transfected group and control group ) and harvested 48 hours later. We used Agilent human 1A oligo microarray identified the changes in gene expression profile of K562 cells after miR-181a transfection experiment. Further studies aimed to find target mRNA of miR-181a in mammalian cells and its biological function. Keywords = miR-181a Keywords = microarray Keywords = K562 Keywords: microRNA transfection analysis
Project description:ETO2 functions as a transcription repressor and is required for the embryonic erythropoiesis and the hemoglobin switch. To gain insight into ETO2 regulatory function during human erythropoiesis, we performed RNA-seq for WT and ETO2 KO K562 cells and found that up-regulated genes upon ETO2 loss in human cells included many markers of mature erythroid cells EPB42, ALAS2, GYPA and SLC25a37. Notably, the α-globin genes (HBA1, HBA2 and HBZ) and embryonic and fetal β-globin genes (HBE1, HBG1, and HBG2) were significantly increased after deletion of ETO2. By contrast, deletion of ETO2 down-regulated the transcription factor genes (ETS1, KLF8 and SOX6) which play a negative role in globin gene expression and hemoglobin synthesis. To further explore different domain function of ETO2, we have analyzed our RNA-seq data from domain deletion cell lines compared to the cell line expressing wild type ETO2. Generally, 702 genes were found to co-regulated by three domain function of ETO2. Interestingly, the regulation of fetal globin genes, erythroid regulator (SOX5) as well as epigenetic factor (HDAC7) is required by three domain function of ETO2. During mouse embryonic erythropoiesis, our FACS-sorted and normal RNA-seq data in E14.5 fetal liver cells indicated that eto2 promoted a critical developmental transition and played an important role in globin switch from embryonic to adult β-globin transcription since its function is essential for key regulators (PU.1, BCL11A and ZBTB7A) and globin genes (Hbb-y and Hba-x) regulation.