Filters
Technology
Platform
GSE34304
Mus musculus, Drosophila melanogaster
30 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Poised RNA polymerase II changes over developmental time and prepares genes for future expression.
Sample Metadata Fields
Specimen part, Cell line, Treatment, Time
View Samples- Mus musculus
- 30 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Murine ES cell gene expression before RA induction are used to compare gene expression for time-points of 8, 12, 16, 24, 36, 48, 60 and 72 hours post-induction.
Publication Title
Poised RNA polymerase II changes over developmental time and prepares genes for future expression.
Sample Metadata Fields
Cell line, Treatment, Time
View Samples- Drosophila melanogaster
- 13 Downloadable Samples
Illumina Genome Analyzer IIx
Description
Poised RNA polymerase II is predominantly found at developmental control genes and is thought to allow their rapid and synchronous induction in response to extracellular signals. How the recruitment of poised RNA Pol II is regulated during development is not known. By isolating muscle tissue from Drosophila embryos at five stages of differentiation, we show that the recruitment of poised Pol II occurs at many genes de novo and this makes them permissive for future gene expression. When compared to other tissues, these changes are stage-specific and not tissue-specific. In contrast, Polycomb group repression is tissue-specific and in combination with Pol II (the balanced state) marks genes with highly dynamic expression. This suggests that poised Pol II is temporally regulated and is held in check in a tissue-specific fashion. We compare our data to mammalian embryonic stem cells and discuss a framework for predicting developmental programs based on chromatin state. Overall design: mRNA-seq of Drosophila tissues during development
Publication Title
Poised RNA polymerase II changes over developmental time and prepares genes for future expression.
Sample Metadata Fields
Specimen part, Subject, Time
View Samples- Homo sapiens
- 12 Downloadable Samples
- IlluminaHiSeq2000
Description
Genetic studies in T-cell acute lymphoblastic leukemia have uncovered a remarkable complexity of oncogenic and loss-of-function mutations. Amongst this plethora of genetic changes, NOTCH1 activating mutations stand out as the most frequently occurring genetic defect, identified in more than 50% of T-cell acute lymphoblastic leukemias, supporting an essential driver role for this gene in T-cell acute lymphoblastic leukemia oncogenesis. In this study, we aimed to establish a comprehensive compendium of the long non-coding RNA transcriptome under control of Notch signaling. For this purpose, we measured the transcriptional response of all protein coding genes and long non-coding RNAs upon pharmacological Notch inhibition in the human T-cell acute lymphoblastic leukemia cell line CUTLL1 using RNA-sequencing. Similar Notch dependent profiles were established for normal human CD34+ thymic T-cell progenitors exposed to Notch signaling activity in vivo. In addition, we generated long non-coding RNA expression profiles (array data) from GSI treated T-ALL cell lines, ex vivo isolated Notch active CD34+ and Notch inactive CD4+CD8+ thymocytes and from a primary cohort of 15 T-cell acute lymphoblastic leukemia patients with known NOTCH1 mutation status. Integration of these expression datasets with publically available Notch1 ChIP-sequencing data resulted in the identification of long non-coding RNAs directly regulated by Notch activity in normal and malignant T-cell context. Given the central role of Notch in T-cell acute lymphoblastic leukemia oncogenesis, these data pave the way towards development of novel therapeutic strategies that target hyperactive Notch1 signaling in human T-cell acute lymphoblastic leukemia. Overall design: CUTLL1 cell lines were treated with Compound E (GSI) or DMSO (solvent control). Cells were collected 12 h and 48 h after treatment. This was performed for 3 replicates. RNA-sequencing was performed on these samples.
Publication Title
The Notch driven long non-coding RNA repertoire in T-cell acute lymphoblastic leukemia.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 19 Downloadable Samples
- NextSeq 500
Description
To identify sex-based differences in gene pathways affected by endgoenous genomic instaiblity resulting in embryonic death, total RNA from E13.5 placentas was isolated for RNAseq. Placentas from male and female embryos from wild-type matings and Mcm4^C3/C3 homozygous matings were used as references. Male and female placentas derived from embryos of the genotype : Mcm4^C3/C3 Mcm2^Gt/+ from either male Mcm4^C3/+ Mcm2^Gt/+ crossed to female Mcm4^C3/C3 or male Mcm4^C3/C3 crossed to female Mcm4^C3/+ Mcm2^Gt/+ were the experimental samples. Overall design: Total RNA was isolated from E13.5 placentas and subjected to directional RNAseq to identify sex-based transciptome differences.
Publication Title
Female-biased embryonic death from inflammation induced by genomic instability.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 4 Downloadable Samples
- Illumina HiSeq 2500
Description
The goal of this study was to identify important genetic pathways that are altered in mammary tumor cells upon over-expression of the tumor suppressor gene Arid1a. The results of this experiment revealed that Arid1a helps regulate key cell-cycle checkpoint and growth regulatory pathways, either directly or indirectly. This helped explain in part the significant decrease in cell proliferation and tumor growth phenotypes observed both in vitro and in vivo, when comparing the same samples analyzed here by RNA-seq (untransduced replicates vs. add-back clonal lines). Overall design: Whole transcriptome comparison of mammary tumor cells derived from Chaos3 mouse model (23116 MT- control) vs. add-back clones overexpressing Arid1a (AB-C1 & AB-C2 - exp). Control and experimental samples were run in duplicate.
Publication Title
The Chromatin Remodeling Component Arid1a Is a Suppressor of Spontaneous Mammary Tumors in Mice.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Homo sapiens
- 90 Downloadable Samples
- Illumina HiSeq 2500
Description
Aim: To discovery biomarkers in JIA base on gene expression from RNA sequencing on PBMC Method: Paired-end Ilumina sequencing to capture gene expression of PBMC from JIA individuals and healthy controls Results:sample heterogeneity makes RNA sequencing on PBMC unsuitable as a first-step method for screening biomarker candidates in JIA Overall design: RNA sequencing on PBMC of 3 independent cohorts consist of JIA patients and healthy controls
Publication Title
Limits of Peripheral Blood Mononuclear Cells for Gene Expression-Based Biomarkers in Juvenile Idiopathic Arthritis.
Sample Metadata Fields
Specimen part, Disease stage, Subject
View Samples- Homo sapiens
- 21 Downloadable Samples
- Illumina HiSeq 2500
Description
Aim: To discovery biomarkers in JIA base on gene expression from RNA sequencing on CD4+ T Cells Method: Paired-end Ilumina sequencing to capture gene expression of CD4+ T cells from JIA individuals with active disease and patients in clinical remission on medication. Overall design: RNA sequencing on CD4+T cells consist of JIA patients
Publication Title
Limits of Peripheral Blood Mononuclear Cells for Gene Expression-Based Biomarkers in Juvenile Idiopathic Arthritis.
Sample Metadata Fields
Specimen part, Disease stage, Subject
View Samples- Homo sapiens
- 45 Downloadable Samples
- Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
Exposure to vanadium pentoxide (V2O5) is a cause of occupational bronchitis. We evaluated gene expression profiles in cultured human lung fibroblasts exposed to V2O5 in vitro in order to identify candidate genes that could play a role in airway remodeling associated with V2O5-induced bronchitis. Gene expression was measured at various time points over a 24 hr period using the Affymetrix Human Genome U133A 2.0 Array. Expression data were preprocessed using RMA with a log2 transformation. Statistical analysis was performed in R using the affylmGUI package using a linear model with contrasts between untreated control and V2O5-exposed fibroblasts. Genes identified as statistically significant were filtered by selecting only those genes that exhibited a > 2-fold change. Quantitative real-time RT-PCR was utilized to confirm expression of selected genes. More than 2000 genes were significantly changed in response to V2O5 over the time course of our experiment. Genes altered by V2O5 were involved in biologic processes related to cell growth and differentiation, oxidative stress responses, immune regulation, and interferon signaling and apoptosis. In particular, V2O5 induced genes that encode growth factors involved in epithelial repair (HB-EGF) or angiogenesis (VEGF), peroxide generating enzymes (SOD2), pro-inflammatory enzymes (PGHS2), while suppressing genes involved in growth arrest (GAS1, STAT-1) and cell cycle inhibition (CDKN1B). Our study also identified a variety of novel genes that could be used as biomarkers of V2O5-induced bronchitis or could serve as candidate genes for disease progression.
Publication Title
Genomic analysis of human lung fibroblasts exposed to vanadium pentoxide to identify candidate genes for occupational bronchitis.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 9 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Recent research has shown that peripheral treatment with amylin reduces Alzheimers disease (AD) pathology in the brain and improves learning and memory in AD mouse models. To understand the mechanism underlying this novel treatment for AD, we interrogated the transcriptome for changes in cortical gene expression in amyloid precursor protein (APP) transgenic mice treated with amylin compared to a vehicle treated group and wild type (WT) mice. Using weighted gene co-expression network analysis, we discovered that amylin treatment influenced two gene modules linked to AD pathology: 1) a module related to proinflammation and transport/vesicle process that included a hub gene of Cd68, and 2) a module related to mitochondria function that included a hub gene of Atp5b. Amylin treatment restored the expression of most genes in the APP cortex toward levels observed in the WT cortex including 23 key hub genes in these two modules. In cultured activated microglia cell line BV-2, we validated that Cd68 expression was attenuated by amylin through binding to the amylin receptor. Using publically-available transcriptomic human data, we found that the expression levels of the orthologues of these hub genes, including Cd68 and Atp5b, strongly correlated with the neurofibrillary tangle burden in the AD brain and with Mini-Mental Status Exam scores. Our study is the first to show the transcriptome-wide targets of amylin treatment, and further supports the potential use of amylin-type peptides to treat AD.
Publication Title
Amylin Treatment Reduces Neuroinflammation and Ameliorates Abnormal Patterns of Gene Expression in the Cerebral Cortex of an Alzheimer's Disease Mouse Model.
Sample Metadata Fields
Specimen part
View Samples