Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

63 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Origins of MLL cancer stem cells govern leukemic self-renewal mediated by -catenin and Hoxa9

ABSTRACT: From mice, strand-specific RNA-Seq of granulocyte-myeloid progenitors (GMP) and hematopoietic stem cells (HSC). Cancer stem cells (CSC) were created with MLL-ENL transfections using puromycin for both GMP and HSCs. Further knock-outs were created of -catenin (Ctnnb1) and Hoxa9.

INSTRUMENT(S): Illumina HiSeq 2000

ORGANISM(S): Mus musculus

SUBMITTER: Bernd Zeisig

PROVIDER: E-MTAB-3647 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Gene expression changes after loss of Hoxa9 in transformed HSCs [HOXA9 RNA-seq]

Project description:Characterization of gene expression changes 72 hours after withdrawal of tamoxifen in murine hematopoietic progenitors transformed by Hoxa9-ER/Meis1 using RNAseq. In the presence of tamoxifen (4OHT), Hoxa9-ER localizes to the nucleus of cells allowing for transformation, while withdrawal of 4OHT (culture in EtOH) leads to loss of nuclear Hoxa9-ER. Loss of Hoxa9-ER leads to a decrease in cellular proliferation and differentiation along the myeloid lineage. Examination of gene expression by RNAseq in two conditions in biological replicates.

2014-06-11 | E-GEOD-58359 | biostudies-arrayexpress

Analysis of transcriptome changes in Kmt2d deletion in cardiac mesoderm, anterior heart field precursors and cardiomyocytes

Project description:KMT2D is required in the cardiac mesoderm, anterior heart field precursors and cardiomyocytes. Kmt2d deletion in cardiac mesoderm (Mesp1Cre) is embryonic lethal at E10.5 and mutants have hypoplastic hearts; Kmt2d deletion in anterior heart field precursors (Mef2cAHF::Cre) deletion is embryonic lethal at E13.5 and mutants have defects in septation of outflow tract and interventricular septum (IVS); Kmt2d deletion in cardiomyocytes (Tnnt2::Cre) deletion is embryonic lethal at E14.5 and mutants have defects in IVS septation and compact myocardium. The goal of this study is to compare changes in gene expression in these Kmt2d conditional deletion mutants and understand common or distinct pathways dysregulated in absence of KMT2D. Whole genome gene expression analysis was performed on RNA isolated from control and mutant embryonic hearts (or right ventricles and outflow tract for anterior heart field deletion samples). Libraries were prepared using Illumina TruSeq Paired-End Cluster Kit v3, and sequenced with the Illumina HiSeq 2500 system for pair-ended 100 base pairs (PE 100 bp).

2015-11-04 | E-GEOD-74679 | biostudies-arrayexpress

Regulation of gene expression through genome-wide co-binding of Hoxa9 and C/EBPα in transformed HSCs

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-06-11 | E-GEOD-58362 | biostudies-arrayexpress

Identification and Characterization of Hoxa9 Binding Sites in Hematopoietic Cells

Project description:The clustered homeobox proteins play crucial roles in development, hematopoiesis and leukemia yet the targets they regulate and their mechanisms of action are poorly understood. Here, we identified the binding sites for Hoxa9 and the Hox cofactor Meis1 on a genome-wide level and profiled their associated epigenetic modifications and transcriptional targets. Hoxa9 and the Hox cofactor Meis1 co-bind at hundreds of highly evolutionarily-conserved sites, most of which are distant from transcription start sites. These sites show high levels of histone H3K4 monomethylation and CBP/P300 binding characteristic of enhancers. Furthermore, a subset of these sites shows enhancer activity in transient transfection assays. Many Hoxa9 and Meis1 binding sites are also bound by PU.1 and other lineage-restricted transcription factors previously implicated in establishment of myeloid enhancers. Conditional Hoxa9 activation is associated with CBP/P300 recruitment, histone acetylation and transcriptional activation of a network of proto-oncogenes including Erg, Flt3, Lmo2, Myb and Sox4. Collectively this work suggests that Hoxa9 regulates transcription by interacting with enhancers of genes important for hematopoiesis and leukemia. To identify the genome-wide binding sites for Hoxa9 and the Hox cofactor Meis1

2011-12-04 | E-GEOD-33509 | biostudies-arrayexpress

RNAseq of murine primary bone marrow cells transformed by an inducible Hoxa9-ER: time-course

Project description:Relative overexpression of HOXA9 is a key feature of aggressive AML (acute myeloid leukemia). Hoxa9 responsive genes were identified by nascent RNA sequencing (4-thio-uridine labeled RNA - sequencing) in samples of primary hematopoietic precursor cells from mice transformed by an tamoxifen inducible version of Hoxa9 (Hoxa9-ER). Samples were generated in the presence of active Hoxa9 (0h) and in a time series after Hoxa9 was inactivated at 8h, 16h, 24h, 48h, and 72h.

2019-04-13 | E-MTAB-7107 | biostudies-arrayexpress

Transcription profiling of mouse adult neural stem cells exogenously expressing Oct4 produces one-factor induced pluripotent stem (1F iPS)

Project description:Pluripotency can be induced in murine and human fibroblast by transduction of four transcription factors (Oct4, Sox2, Klf4 and c-Myc). Previously we reported that two factors (Oct4 and Klf4) are sufficient for reprogramming adult mouse neural stem cells (NSCs) to a pluripotent state. However, although NSCs endogenously express the factors Sox2, c-Myc, and Klf4, our previous report does not elucidate why exogenous expression of either Klf4 or c-Myc is still required for reprogramming. Here we report that exogenous expression of Oct4 is sufficient to generate one-factor induced pluripotent stem (1F iPS) cells without any oncogenic factors, such as c-Myc and Klf4, from mouse adult NSCs, which endogenously express Sox2, c-Myc, and Klf4, and also intermediate reprogramming markers alkaline phosphatase (AP), stage-specific embryonic antigen-1 (SSEA-1). These results extend our previous report proposing that somatic cells can be reprogrammed to a pluripotent state with a reducing number of reprogramming factors when the complementing factors are endogenously expressed in the somatic cells. Experiment Overall Design: 10 hybridizations in total. Experiment Overall Design: NSC-derived iPS cells by one-factor (Oct4) in triplicate: Experiment Overall Design: - NSC_1F_iPS_1 Experiment Overall Design: - NSC_1F_iPS_2 Experiment Overall Design: - NSC_1F_iPS_3 Experiment Overall Design: One-factor (Oct4) iPS cell-derived NSC in triplicate: Experiment Overall Design: - 1F_iPS_NSC_1 Experiment Overall Design: - 1F_iPS_NSC_2 Experiment Overall Design: - 1F_iPS_NSC_3 Experiment Overall Design: Neural stem cell (NSC) derived from brain of OG2/Rosa26 mice: Experiment Overall Design: - NSC_1 Experiment Overall Design: - NSC_2 Experiment Overall Design: - NSC_3 Experiment Overall Design: - NSC_4

2009-02-08 | E-GEOD-12499 | biostudies-arrayexpress

Transcription profiling of mouse vehicle and sAPPalpha-treated hippocampal slice cultures

Project description:Gene expression changes induced by alpha-secretase cleaved amyloid precursor protein (sAPPalpha) in organotypic hippocampal slice cultures of male, postnatal day 15 mice (C57B6/SJL). Hippocampal slice cultures were treated with phosphate buffered saline (GSM26700, GSM26701, GSM26702) or 1 nM sAPPalpha (GSM26703, GSM26704, GSM26705) for 24 h. Each sample consists of total RNA isolated from 8-12 slices from 4 mice. Data were analyzed with MAS 5.0 and scaled to 2500. sAPPalpha induces the amyloid sequestration protein transthyretin, insulin-like growth factor 2, insulin-like growth factor binding protein 2, and other genes involved in protective pathways such as apoptosis inhibition, detoxification, and retinol transport. See Stein, TD, Anders, NJ, DeCarli, C, Chan, SL, Mattson, MP, and Johnson JA. Neutralization of transthyretin reverses the neuroprotective effects of secreted APP in APPSw mice resulting in tau phosphorylation and loss of hippocampal neurons: support for the amyloid hypothesis. J Neurosci. in press.

2007-10-10 | E-GEOD-1555 | biostudies-arrayexpress

Tet2-/-Flt3ITD and WT stem and progenitor cells

Project description:The study was a comparison of gene expression using RNA-seq. We analyzed the stem and progenitor cells from WT and Vav-cre+ Tet2fl/fl Flt3-ITD (T2F3) mice. We isolated stem cells LSK (lin- sca+ kit+) and granulocyte-macrophage progenitors GMP (lin- sca- kit+ fcgr+ cd34+) cells from bone marrow. Comparisons were made across genotypes WT vs. T2F3 and cell types LSK vs. GMP. Comparison of WT and Tet2-/-Flt3ITD bone marrow stem and progenitor cells.

2015-05-01 | E-GEOD-57244 | biostudies-arrayexpress

LRH-1 and PTF1-L coregulate an exocrine pancreas-specific transcriptional network for digestive function [RNA-Seq]

Project description:Two separate pools of three Flox or two Lrh1t-/- pancreas RNA preparations was subjected to the Illumina RNA-seq protocol. Examination of mRNA levels in induced Lrh1 pancreas knockout and wild-type mice.

2011-11-30 | E-GEOD-34030 | biostudies-arrayexpress

LRH-1 and PTF1-L coregulate an exocrine pancreas-specific transcriptional network for digestive function [ChIP-Seq]

Project description:We have determined the cistrome and transcriptome for the nuclear receptor liver receptor homolog-1 (LRH-1) in the exocrine pancreas. Chromatin immunoprecipitation (ChIP)-seq and RNA-seq analyses reveal that LRH-1 directly induces expression of genes encoding digestive enzymes and secretory and mitochrondrial proteins. LRH-1 cooperates with the pancreas transcription factor 1-L complex (PTF1-L) in regulationg exocrine pancreas-specific gene expression. Elimination of LRH-1 in adult mice reduced the concentration of several lipases and proteases in pancreatic fluid and impaired pancreatic fluid secretion in response to cholecystokinin. Thus, LRH-1 is a key regulator of the exocrine pancreas-specific transcriptional network required for the production and secretion of pancreatic fluid. input and Lrh1 ChIP

2011-12-09 | E-GEOD-34295 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data