Filters
Technology
Platform
SRP090333
Homo sapiens
20 Downloadable Samples
Illumina HiSeq 2500
Description
RUNX1 is a frequent target of translocations in acute myeloid leukemia whereby its DNA binding domain fuses to different epigenetic regulators. To assess how different RUNX1 fusion proteins interact with the epigenome we compared the global binding patterns and the chromatin landscape of t(8;21) and t(3;21) AML which express RUNX1-ETO and RUNX1-EVI-1, respectively. We found that differential prognosis for these types of AML is reflected in fundamental differences in gene expression, chromatin landscape, binding patterns of the fusion proteins and other transcription factors as identified by genome-wide digital footprinting in patients. As previously shown for RUNX1-ETO, knockdown of RUNX1-EVI-1 expression initiates differentiation of t(3;21) cells which is associated with up-regulation of genes vital for myeloid differentiation, including C/EBPa. Furthermore, by expressing either dominant-negative C/EBP or an inducible C/EBPa construct in t(3;21) cells we show that C/EBPa is necessary and sufficient for the differentiation response of these cells to RUNX1-EVI-1 knockdown. Overall design: RNA-seq expreiments have been used to study the chromatin landscape of t(8;21) and t(3;21) AML
Publication Title
RUNX1-ETO and RUNX1-EVI1 Differentially Reprogram the Chromatin Landscape in t(8;21) and t(3;21) AML.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 55 Downloadable Samples
Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Gaucher disease: transcriptome analyses using microarray or mRNA sequencing in a Gba1 mutant mouse model treated with velaglucerase alfa or imiglucerase.
Sample Metadata Fields
Age, Specimen part, Treatment
View Samples- Mus musculus
- 54 Downloadable Samples
- Illumina HiSeq 2000
Description
The comparative whole genome transcriptome effects of two similar pharmaceuticals, imig or vela, on a Gaucher disease mouse model, 9V/null, were evaluated by two commonly used platforms, mRNA-Seq and microarray. Also, statistical methods, DESeq and edgeR for mRNA-Seq and Mixed Model ANOVA for microarray, were compared for differential gene expression detection. The biological pathways were similar between two platforms. Cell growth and proliferation, cell cycle, heme metabolism, and mitochondrial dysfunction were the most altered functions associated with the disease process. Although the two biopharmaceuticals have a very similar structure and function, imig- and vela- treatment in the mice differentially affected disease-specific pathways indicating the action of the two drugs on the disease process in the visceral tissues of Gaucher mouse model differ significantly at the molecular level. This study provides a comprehensive comparison between the two platforms (mRNA-Seq and microarray) for gene expression analysis and addresses the contribution of the different methods involved in the analysis of such data. The results also provide insights into the differential molecular effects of two similar biopharmaceuticals for Gaucher disease treatment Overall design: 9V/null mice (Gaucher mouse model) were injected weekly via tail vein with 60U/kg/wk of imig or vela for 8 wks. Control 9V/null mice were injected with same volume of saline. Wt mice were untreated. Age and strain matched mice were used for the study. Also, statistical methods, DESeq and edgeR for mRNA-Seq and Mixed Model ANOVA for microarray, were compared for differential gene expression detection. Cell growth and proliferation, cell cycle, heme metabolism, and mitochondrial dysfunction were the most altered functions associated with the disease process. The results also provide insights into the differential molecular effects of two similar biopharmaceuticals for Gaucher disease treatment.
Publication Title
Gaucher disease: transcriptome analyses using microarray or mRNA sequencing in a Gba1 mutant mouse model treated with velaglucerase alfa or imiglucerase.
Sample Metadata Fields
Age, Specimen part, Treatment, Subject
View Samples- Mus musculus
- 24 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Gaucher disease: transcriptome analyses using microarray or mRNA sequencing in a Gba1 mutant mouse model treated with velaglucerase alfa or imiglucerase.
Sample Metadata Fields
Age, Specimen part, Treatment
View Samples- Mus musculus
- 24 Downloadable Samples
- Illumina HiSeq 2000
Description
Gaucher disease type 1 is an inborn error of metabolic disease with the defective activity of the lysosomal enzyme acid b-glucosidase (GCase). Enzyme replacement/reconstitution therapy (ERT), infusions with purified recombinant GCases, is efficacious in reversing hematologic, hepatic, splenic, and bony disease manifestations in Gaucher type 1 patients. However, the tissue specific molecular events in Gaucher disease and their response to therapy are not known yet. To explore the molecular events underlying GCase treatment, we evaluated the tissue-specific gene expression profiles and molecular responses in our Gaucher disease mouse model, which were treated with two FDA approved commercially available GCases, imiglucerase (imig) and velaglucerase alfa (vela). Using microarray and mRNA-Seq techniques, differentially expressed genes (DEGs) were identified in the spleen and liver by the direct comparison of imig- vs. vela- treated mice. Among them three gene expression networks were derived from these spleens: 1) cell division/proliferation, 2) hematopoietic system and 3) inflammatory/macrophage response. Our study showed the occurrence of differential molecular pathophysiologic processes in the mice treated with imig compared with vela even though these two biosimilars had the same histological and biochemical efficacy Overall design: 9V/null mice (Gaucher mouse model) were injected weekly via tail vein with 60U/kg/wk of imig or vela for 8 wks. To understand the molecular events underlying GCase treatment, we evaluated the tissue-specific gene expression profiles and molecular responses in our Gaucher disease mouse model, which were treated with two FDA approved commercially available GCases, imiglucerase (imig) and velaglucerase alfa (vela).
Publication Title
Gaucher disease: transcriptome analyses using microarray or mRNA sequencing in a Gba1 mutant mouse model treated with velaglucerase alfa or imiglucerase.
Sample Metadata Fields
Age, Specimen part, Treatment, Subject
View Samples- Mus musculus
- 3 Downloadable Samples
- Illumina HiSeq 2000
Description
Purpose: The aim of this study is to determine the relative expresson levels of mRNA transcripts in wild type platelets Methods: Total RNA was extracted and purified from purified platelets from BALB/c male mice (3 independent samples). Platelet purification was performed as described in Josefsson EC et al, Journal of Experimental Medicine (2011) 208:2017-31. Total RNA (100 ng) was used to generate sequencing libraries for whole transcriptome analysis following Illumina’s TruSeq RNA v2 sample preparation protocol. Completed libraries were sequenced on HiSeq 2000 with TruSeq SBS Kit v3- HS reagents (Illumina) as 100 bp paired-end reads at the Australian Genome Research Facility (AGRF), Melbourne. Reads were aligned to the mouse reference genome mm10 and counts for known genes were obtained using the Rsubread package (version 1.18.0) (Liao et al. 2013; Liao et al. 2014). Overall design: Total RNA was extracted and purified from purified platelets from BALB/c male mice (3 independent samples per population).
Publication Title
Loss of PUMA (BBC3) does not prevent thrombocytopenia caused by the loss of BCL-XL (BCL2L1).
Sample Metadata Fields
Age, Specimen part, Cell line, Subject
View Samples- Homo sapiens
- 12 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
Analysis of genes that were differentially expressed in axolotl extract reprogrammed tumour xenografts compared to untreated controls. The study provided insight into the biological processes, signalling pathways and gene networks affected by the oocyte extract treatment which resulted in halted tumour growth in mice.
Publication Title
Cancer reversion with oocyte extracts is mediated by cell cycle arrest and induction of tumour dormancy.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Homo sapiens
- 51 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Differencies between groups between pre and post haematopoietic stem cell transplantation children
Publication Title
Genetic Background of Immune Complications after Allogeneic Hematopoietic Stem Cell Transplantation in Children.
Sample Metadata Fields
Specimen part, Disease stage
View Samples- Homo sapiens
- 9 Downloadable Samples
- Illumina HumanRef-8 v3.0 expression beadchip
Description
Based on the results of numerous clinical and preclinical analyses, the transcription factor HIF-1a has been identified as an important tumor-promoting factor and is considered to be an attractive target for cancer therapy. To further deconstruct the molecular nature of HIF-1as role in tumorigenesis, we have applied lentiviral shRNA transduction to establish HIF-1a-deficient gastric cancer cells. Interestingly, functional analyses failed to show a significant growth defect of HIF-1a-deficient gastric cancer cells in vitro and in vivo. These observations led us to propose that stable inactivation of HIF-1a resulted in efficient compensation enabling cell growth and, ultimately, tumor progression in a HIF-1a-independent manner. To better understand the mechanisms that control this compensation, we performed transcriptomics of control (scrambled (SCR)) and HIF-1a-deficient (HIF) gastric cancer cells.
Publication Title
Annexin A1 sustains tumor metabolism and cellular proliferation upon stable loss of HIF1A.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus
- 68 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Prosaposin encodes, in tandem, four small acidic activator proteins (saposins) with specificities for glycosphingolipids hydrolases in lysosomes. To explore the molecular mechanism(s) of disease progression, temporal transcriptome microarray analyses of cerebrum and cerebellum tissues were conducted using mRNA from three prosaposin deficiency mouse models: PS-NA (hypomorphic prosaposin deficiency), PS-/- (prosaposin null) and 4L/PS-NA (a V394L/V394L glucocerebrosidase mutation and PS-NA) mice. Our results indicate that regionally specific gene expression abnormalities preceded the histological and behavioral changes and CEBPD is a candidate regulator of brain disease in prosaposin deficiency. The alterations of gene expression are detected at birth and are more profound in cerebellum than cerebrum.
Publication Title
Temporal gene expression profiling reveals CEBPD as a candidate regulator of brain disease in prosaposin deficient mice.
Sample Metadata Fields
No sample metadata fields
View Samples