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RNAi expression experiments on Illumina BeadChip

ABSTRACT: Mouse embryonic stem cells (mES) were depleted of Klf2, Klf4, and Klf5 by ectopic expression of shRNA. Control RNAi was performed using shRNA against luciferase. At 2 days, 4 days and 6 days post-transfection of shRNA-encoding vectors, cells are harvested for RNA isolation. Keywords: RNAi expression, Mouse ES cells

ORGANISM(S): Mus musculus

PROVIDER: GSE9775 | GEO | 2008/02/11

SECONDARY ACCESSION(S): PRJNA105113

REPOSITORIES: GEO

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RNAi expression experiments on Illumina BeadChip

Project description:Mouse embryonic stem cells (mES) were depleted of Klf2, Klf4, and Klf5 by ectopic expression of shRNA. Control RNAi was performed using shRNA against luciferase. At 2 days, 4 days and 6 days post-transfection of shRNA-encoding vectors, cells are harvested for RNA isolation. Keywords: RNAi expression, Mouse ES cells Knockdown: Klf2, Klf4, Klf5, Luciferase (Control);Time: 2 days post-transfection, 4 days post-transfection, 6 days post-transfection;Three independent experimental replicates for each experimental condition were performed.

2010-06-25 | E-GEOD-9775 | biostudies-arrayexpress

ChIP-chip on custom NimbleGen genomic tiling arrays

Project description:Performing Chromatin IP of Klf2, Klf4, Klf5 and p53 in mouse embryonic stem cells with NimbleGen custom genomic tiling arrays, we sought to decipher Klf2, Klf4, Klf5-regulated genes. 12 samples: Chromatin IP of Klf2, Klf4, Klf5 and p53 in mouse embryonic stem cells with NimbleGen custom genomic tiling arrays; three independent experimental replicates for each experimental condition were performed.

2010-05-26 | E-GEOD-9774 | biostudies-arrayexpress

Strome MES-4, H3K36me3 and H3K27me3 in mes-4 RNAi EEMB

Project description:ChIP-chip of MES-4, H3K36me3 and H3K27me3 in mes-4 RNAi C. elegans early embryo

2012-05-30 | GSE38159 | GEO

Identifying targets of Klf2, Klf4, Klf5 and p53 in mouse embryonic stem cells

Project description:This SuperSeries is composed of the following subset Series: GSE9774: Klf2, Klf4, Klf5 and p53 in mouse embryonic stem cells GSE9775: To identify the target genes of Klf2, Klf4 and Klf5 in mouse embryonic stem cells. Keywords: SuperSeries Refer to individual Series

2010-06-25 | E-GEOD-9535 | biostudies-arrayexpress

ChIP-chip on custom NimbleGen genomic tiling arrays

2008-02-11 | GSE9774 | GEO

Strome MES-4, H3K36me3 and H3K27me3 in mes-4 RNAi EEMB

Project description:ChIP-chip of MES-4, H3K36me3 and H3K27me3 in mes-4 RNAi C. elegans early embryo EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: mes-4 RNAi; Developmental Stage: Early Embryo; Genotype: N2; Sex: population predominantly Hermaphrodites perhaps with some Males; NUMBER OF REPLICATES: 2; EXPERIMENTAL FACTORS: temperature 24

2012-05-29 | E-GEOD-38159 | biostudies-arrayexpress

MYBL2 Is a Sub-haploinsufficient Tumor Suppressor Gene in Myeloid Malignancy (RNAi)

Project description:A dosage-dependent role for tumor suppressor genes in the initiation of myeloid malignancies remains controversial. Here we show that MYBL2 is expressed at sharply reduced levels in CD34+ cells from most patients with myelodysplastic syndrome (MDS; 65%; n=26). In a murine competitive reconstitution model, Mybl2 knockdown by RNAi to 20-30% of normal levels in multipotent hematopoietic progenitors led to clonal dominance by these M-bM-^@M-^\sub-haploinsufficientM-bM-^@M-^] cells, affecting all blood cell lineages. By 6 months post-transplantation, the reconstituted mice had developed a myeloproliferative/myelodysplastic disorder originating from the cells with aberrantly reduced Mybl2 expression. Thus, downregulation of MYBL2 activity to levels below those predicted by classical haploinsufficiency drives the clonal expansion of hematopoietic progenitors in a large fraction of human MDS cases. Cryopreserved CD34+ bone marrow were cultured for 24 hours, transduced with shRNA-encoding vectors and selected with Puromycin for 48 hours. Vectors shRNA 1-8 are specifically targeting MYBL2, vectors shRNA A-D encoded an irrelevant control shRNAs and one culture was left untreated (no shRNA). Cells were harvested after Puromycin selection and total RNA was prepared using Trizol (LifeTechnologies).

2013-09-15 | E-GEOD-43400 | biostudies-arrayexpress

lin-35(n745) mutants vs. lin-35(n745), mes-4(RNAi) (below referred to as reference sample and test sample respectively)

Project description:Transcriptional profiling of C. elegans first larval stage whole animals comparing lin-35(n745) mutants and lin-35(n745) treated with mes-4(RNAi) at 26 degrees. One-condition experiment, mutant (lin-35) vs. mutant plus RNAi (lin-35, mes-4RNAi). Biological replicates 4 mutant, 4 mutant plus RNAi harvested indepedently. One lin-35 replicate and one lin-35, mes-4(RNAi) replicate per array.

2011-01-25 | E-GEOD-26825 | biostudies-arrayexpress

lin-35(n745) mutants vs. lin-35(n745), mes-4(RNAi) (below referred to as reference sample and test sample respectively)

Project description:Transcriptional profiling of C. elegans first larval stage whole animals comparing lin-35(n745) mutants and lin-35(n745) treated with mes-4(RNAi) at 26 degrees.

2011-01-25 | GSE26825 | GEO

Genome-scale analysis in blood progenitor and mast cells reveals how lineage-affiliated transcription factors control distinct regulatory programs [Beadchip Experiments]

Project description:Despite major advances in the generation of genome-wide binding maps, the mechanisms by which transcription factors (TFs) regulate cell type identity have remained largely obscure. Through comparative analysis of 10 key haematopoietic TFs in both mast cells and blood progenitors, we demonstrate that the largely cell-type specific binding profiles are not opportunistic, but instead contribute to cell-type specific transcriptional control, because (1) mathematical modelling of differential binding of shared TFs can explain differential gene expression, (2) cell-type specific binding is largely mediated through consensus binding sites, and (3) knock-down of blood stem cell regulators Gata2 and Erg in mast cells reveals mast cell specific genes as direct targets. Finally we show that the known mast cell regulators Mitf and c-Fos likely contribute to the global reorganisation of TF binding profiles. Taken together therefore, our study elucidates how key regulatory TFs contribute to transcriptional programmes in several distinct mammalian cell types. Total RNA from primary mast cells transfected with retroviral shRNA vectors were compared to negative controls (shRNA against luciferase).

2014-04-24 | E-GEOD-47988 | biostudies-arrayexpress

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