Project description:The ensemble of Foxo3-regulated genes in the erythroid G1E-ER-GATA-1 cell line was determined by knocking down Foxo3 using siRNA, and measuring genome wide transcription by microarray analysis G1E-ER-GATA-1 cells were treated with control or Foxo3-specific siRNA by nucleofection at t = 0 h and t = 24 h. At t = 24 h, cells were treated with M-CM-^_-estradiol to activate ER-GATA-1. RNA was harvested at t = 48 h and processed for microarray analysis.
Project description:Total RNA was analyzed from either uninduced or β-estradiol treated G1E-ER-GATA cells to determine changes in gene expression upon induction of erythroid maturation (treated).
Project description:This SuperSeries is composed of the following subset Series: GSE24333: Expression data from ETO2 knockdown G1E-ER-GATA-1 cells GSE24336: Expression data from LMO2 knockdown G1E-ER-GATA-1 cells Refer to individual Series
Project description:Identification of genes regulated by GATA-1 independent of the cofactor FOG-1. Experiment Overall Design: A conditionally activated FOG-1-binding defective mutant of GATA-1, ER-GATA-1(V205G), was expressed in GATA-1-null G1E cells. Transcipt levels were compared in cells untreated or treated with estradiol to activate the GATA-1 mutant.
Project description:We used microarrays to examine what genes could be regurated by LMO2 in erythroid cells. Comparing expression profile in murine G1E-ER-GATA-1 cells treated with control and Lmo2 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: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:Alas2 gene encodes the rate-limiting enzyme in heme biosynthesis. CRISPR/Cas9-mediated ablation of two Alas2 intronic cis-elements strongly reduced GATA-1-induced Alas2 transcription, heme biosynthesis, and GATA-1 regulation of other vital constituents of the erythroid cell transcriptome. Bypassing Alas2 function in Alas2 cis-element-mutant (double mutant) cells by providing its catalytic product 5-aminolevulinic acid (5-ALA) rescued heme biosynthesis and the GATA-1-dependent genetic network. We discovered a GATA factor- and heme-dependent circuit that establishes the erythroid cell transcriptome. G1E-ER-GATA-1 WT and double mutant cells were examined. Untreated WT, beta-estradiol-treated WT, beta-estradiol-treated double-mutant, and beta-estradiol/5-ALA-treated double-mutant cells were subjected to RNA-seq.
