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Expresssion data in K562 cells, before and after TPA induction and including a RUNX1 knockout construct or a control structure

ABSTRACT: Expresssion data in K562 cells, before and after TPA induction and including a RUNX1 knockout construct or a control structure Examination of gene expression in K562 cells, before and following TPA induction and with or without a RUNX1 KO construct or control

ORGANISM(S): Homo sapiens

SUBMITTER: Ram Jaschek

PROVIDER: E-GEOD-24778 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Dynamic combinatorial interactions of RUNX1 and cooperating partners regulates megakaryocytic differentiation in cell line models.

Pencovich Niv N Jaschek Ram R Tanay Amos A Groner Yoram Y

Blood 20101019 1

Specific interactions of transcription factors (TFs) with their targets are crucial for specifying gene expression programs during cell differentiation. How specificity is maintained despite limited selectivity of individual TF-DNA interactions is not fully understood. RUNX1 TF is among the most frequently mutated genes in human leukemia and an important regulator of megakaryopoiesis. We used megakaryocytic cell lines to characterize the network of RUNX1 targets and cooperating TFs in differenti ...[more]

PMID: 20959602

Similar Datasets

Dynamic combinatorial interactions of RUNX1 and cooperating partners regulates megakaryocytic differentiation in cell line models

Project description:This SuperSeries is composed of the following subset Series: GSE24777: Regulation of Megakaryocytic differentiation in Cell Line Models by Dynamic Combinatorial Interactions of RUNX1 with Its Cooperating Partners GSE24778: Expresssion data in K562 cells, before and after TPA induction and including a RUNX1 knockout construct or a control structure Refer to individual Series

2011-01-10 | E-GEOD-24779 | biostudies-arrayexpress

Regulation of Megakaryocytic differentiation in Cell Line Models by Dynamic Combinatorial Interactions of RUNX1 with Its Cooperating Partners

Project description:Regulation of Megakaryocytic differentiation in Cell Line Models by Dynamic Combinatorial Interactions of RUNX1 with Its Cooperating Partners Examination of RUNX1 binding in K562 cells, before and following TPA induction and CMK cells. Examination of GATA1 and FOS binding and H3K4me1 and H3K27me3 modification levels following TPA induction in K562 cells.

2011-01-10 | E-GEOD-24777 | biostudies-arrayexpress

Expresssion data in K562 cells, before and after TPA induction and including a RUNX1 knockout construct or a control structure

Project description:Expresssion data in K562 cells, before and after TPA induction and including a RUNX1 knockout construct or a control structure

2011-01-10 | GSE24778 | GEO

Small RNA sequencing of human K562 cells transduced with lentiviral vectors overexpressing RUNX1

Project description:miRNA-Sequencing of RUNX1 overexpressing K562 cells were compared to K562 cells transduced with an empty vector control to analyse the differential expression of miRNAs in hematopoiesis. K562 cells were transduced either with an empty lentiviral vector as control or a lentiviral vector overexpressing human RUNX1. The samples were biological triplicates and the results were validated by qRT-PCR using SYBR green.

2016-06-01 | E-GEOD-70942 | biostudies-arrayexpress

Transcription profiling of human erythroleukemia K562 cells during TPA-induced megakaryocyte differentiation

Project description:Analysis of differential gene expression during TPA-induced megakaryocyte differentiation of human erythroleukemia K562 cells. The transcription profile of untreated vs TPA-treated K562 cells for 2 days was compared using gene microarrays.

2009-09-01 | E-MEXP-2213 | biostudies-arrayexpress

Transcription profiling of human K562 cells overexpressing miR-34a

Project description:miR-34a is strongly induced upon TPA-induced megakaryocyte differentiation of K562 cells. To investigate the gene networks regulated by this miRNA during the process of differentiation we performed gene microarray analysis in K562 cells overexpressing miR-34a or a control sequence. Experiment Overall Design: K562 cells were transfected by nucleofection (Amaxa) with a miR-34a mimic (Dharmacon) or a control sequence with no homology to human genes. 24 hours post-transfection total RNA was extracted using trizol and hybridized on Affimetrix microarrays for comparing gene expression.

2009-07-19 | E-GEOD-16674 | biostudies-arrayexpress

Pro-seq of shControl and shRUNX1-ETO Kasumi-1 cells

Project description:RUNX1-ETO knockdown was performed in Kasumi-1 cells and Pro-seq analyses were performed. Control cells (Kasumi-1 shControl) were also analysed and all samples were analysed in duplicates.

2022-02-01 | E-MTAB-9019 | biostudies-arrayexpress

Transcriptomic analysis of imatinib-resistant K562 cells with knocked down Pleomorphic Adenoma Gene 1 (PLAG1) to identify the targets

Project description:Genomic profiling of K562 cells resistant to imatinib as well as imatinib resistant CML patients harboured a recurrent chromosomal amplification in 8q11.2-12.1. Gene encoding PLAG1, a transcription factor associated with cancers and chemo resistance, resides on this locus and was found to be amplified in resistant cells. Upon PLAG1 knockdown we observed a decrease in imatinib resistance, and to understand the molecular events underlying PLAG1-mediated imatinib resistance, RNA sequencing was carried out. Imatinib-resistant K562 cells were transfected with lentiviral particles containing shRNA against PLAG1 and lentiviral particles containing pLKO.1-empty vectors. Monoclonal populations were established. Total RNA sequencing was performed. For QC, RNA samples were quantified using the Qubit RNA BR Assay kit (Invitrogen, Cat# Q10211). RNA purity was checked using QIAxpert, and RNA integrity was assessed on TapeStation using High Sensitivity RNA ScreenTape® (Agilent, Cat# 5067-5579). QC passed RNA samples were subjected to the library preparation, and NEB Ultra RNA-Seq Library Prep kit protocol (Cat# E7530L) was used and sequenced on Illumina NovaSeq 6000 instrument. Transcriptomic analysis identified several genes down-regulated upon PLAG1 knockdown which were further investigated.

2024-01-01 | E-MTAB-11893 | biostudies-arrayexpress

RUNX1 contributes to higher-order chromatin organization and gene regulation in breast cancer cells.

Project description:RUNX1 is a transcription factor functioning both as an oncogene and a tumor suppressor in breast cancer. RUNX1 alters chromatin structure in cooperation with chromatin modifier and remodeling enzymes. In this study, we examined the relationship between RUNX1-mediated transcription and genome organization. We characterized genome-wide RUNX1 localization and performed RNA-seq and Hi-C in RUNX1-depleted and control MCF-7 breast cancer cells. RNA-seq analysis showed that RUNX1 depletion led to up-regulation of genes associated with chromatin structure and down-regulation of genes related to extracellular matrix biology, as well as NEAT1 and MALAT1 lncRNAs. Our ChIP-Seq analysis supports a prominent role for RUNX1 in transcriptional activation. About 30% of all RUNX1 binding sites were intergenic, indicating diverse roles in promoter and enhancer regulation and suggesting additional functions for RUNX1. Hi-C analysis of RUNX1-depleted cells demonstrated that overall three-dimensional genome organization is largely intact, but indicated enhanced association of RUNX1 near Topologically Associating Domain (TAD) boundaries and alterations in long-range interactions. These results suggest an architectural role for RUNX1 in fine-tuning local interactions rather than in global organization. Our results provide novel insight into RUNX1-mediated perturbations of higher-order genome organization that are functionally linked with RUNX1-dependent compromised gene expression in breast cancer cells. Hi-C and RNA-seq experiments were conducted in MCF-7 shNS and shRUNX1 cells. RUNX1 ChIP-seq was conducted in wildtype MCF-7 cells.

2016-08-23 | E-GEOD-75070 | biostudies-arrayexpress

A novel small-molecule inhibitor of STAT5A/STAT5B with therapeutic potential for prostate cancer and CML

Project description:We assessed the gene expression profiles induced by both genetic and pharmacological knockdown of Stat5a/b in CML cells. Stat5 was suppressed in K562 cells by lentiviral expression of Stat5 shRNA vs. scramble control for 6 days or by treatment of the cells with IST5-002 (5 µM) for 48 h. K562 cells were treated with IST5-002 (5 µM) or vehicle (DMSO) for 48 h. For Stat5 knockdown, K562 cells were infected with Stat5-shRNA lentivirus or scramble-shRNA lentivirus (as control) for 48 h followed by puromycin (2ug/ml) selection for 6 days to enrich for cells expressing Stat5 or scramble shRNA. Each group (vehicle control, IST5-002, scramble-shRNA control and Stat5-shRNA) was prepared in triplicate, and RNA samples from each group were not pooled.

2015-07-01 | E-GEOD-61312 | biostudies-arrayexpress

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