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GSE62156
Homo sapiens
64 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Genetic studies have shown that human T-ALLs can be divided into subgroups that are characterized by unique gene expression signatures and relate to stages of T-cell differentiation at which the leukemic cells arrest. Each molecular subgroup has characteristic genetic abnormalities that cause aberrant activation of specific T-ALL transcription factor oncogenes, including LYL1/MEF2C, HOXA, TLX1, TLX3 and TAL1/LMO2. Notably, the recently described Early T-cell Precursor ALL (ETP-ALL) patients have leukemic cells that show an early block in T-cell differentiation and significantly overlap with LYL1-positive T-ALL and MEF2C-dysregulated immature T-ALL. We studied the gene expression profiles of 64 primary T-ALL samples and found a high BCL-2 expression in immature T-ALL patients compared to patients belonging to other subgroups.
Publication Title
ABT-199 mediated inhibition of BCL-2 as a novel therapeutic strategy in T-cell acute lymphoblastic leukemia.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 27 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Human disease caused by highly pathogenic avian influenza (HPAI) H5N1 can lead to a rapidly progressive viral pneumonia leading to acute respiratory distress syndrome. There is increasing evidence suggests a role for virus-induced cytokine dysregulation in contributing to the pathogenesis of human H5N1 disease. The key target cells for the virus in the lung are the alveolar epithelium and alveolar macrophages, and previous data has shown that compared to seasonal human influenza viruses, equivalent infecting doses of H5N1 viruses markedly up-regulate pro-inflammatory cytokines in both primary cell types in vitro. The dysregulation of H5N1-induced host responses is therefore important for understanding the viral pathogenesis.
Publication Title
Systems-level comparison of host-responses elicited by avian H5N1 and seasonal H1N1 influenza viruses in primary human macrophages.
Sample Metadata Fields
Specimen part, Subject, Time
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
Our results indicate that oxidation of TAF10 by LOXL2 induces its release from its promoters, leading to a block in TFIID-dependent gene transcription. Since TFIID complex is crucial for the expression of Nanog, Klf4, Sox2 and Oct4 and for maintaining the pluripotent state of embryonic stem cells, TAF10 oxidation by LOXL2 leads to inactivation of the pluripotency genes and a loss of pluripotent capacity in embryonic stem cells. Moreover, in vivo results demonstrate an essential role of LOXL2 in neural differentiation during zebrafish development: in the absence of LOXL2 the neural progenitor gene Sox2 is aberrantly overexpressed and neural differentiation is impaired.
Publication Title
LOXL2 Oxidizes Methylated TAF10 and Controls TFIID-Dependent Genes during Neural Progenitor Differentiation.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 80 Downloadable Samples
Illumina HiSeq 2000
Description
The multiple claims about reactivation of the embryonic stem cell (ESC) pluripotency factor OCT4 in somatic cells are highly controversial due to the fact that there is no direct evidence that OCT4 has a functional role in cells other than ESCs. Herein we demonstrate that smooth muscle cell (SMC)-specific knockout of Oct4 within atherosclerotic mice resulted in increased lesion size and multiple changes consistent with decreased plaque stability. SMC-lineage tracing studies showed that lesions from SMC-specific conditional Oct4 KO mice had a reduced number of SMCs likely due to impaired SMC migration. RNA-seq analysis of lesion specimens showed that loss of Oct4 in SMCs was associated with marked activation of genes associated with inflammation and suppression of genes associated with cell migration, a number of which were shown to be activated in cultured SMCs by the combination of hypoxia and oxidized phospholipids in an OCT4-dependent manner. Activation of Oct4 within SMCs was associated with hydroxymethylation of the Oct4 promoter and was HIF1a- and KLF4-dependent. Results provide the first genetic evidence that OCT4 plays a functional role in somatic cells and highlight the importance of further investigation of possible OCT4 functions in somatic cells. Overall design: In vivo: mRNA profiles of 18 week fed Western diet wild type (WT) and Oct4-/- mice were generated by deep sequencing, four animals per group, using Illumina HiSeq 2000. In vitro: a smooth muscle cell wild type (WT) and Oct4-/- (KO) primary aortic cell line was generated and used. mRNA profiles were generated by deep sequencing, in triplicates, using Illumina HiSeq 2000, for the following groups: WT-normoxia-vehicle; WT-normoxia-POVPC; KO-normoxia-vehicle; KO-normoxia-POVP; WT-hypoxia-vehicle; WT-hypoxia-POVPC; KO-hypoxia-vehicle; and KO-hypoxia-POVPC.
Publication Title
Perivascular cell-specific knockout of the stem cell pluripotency gene Oct4 inhibits angiogenesis.
Sample Metadata Fields
Specimen part, Cell line, Treatment, Subject
View Samples- Mus musculus
- 24 Downloadable Samples
- Illumina HiSeq 2500
Description
Background: Increasing evidence indicates stem cell transplantation may be an effective stroke treatment but little is known about the direct impact of transplanted cells on injured brain tissue. We investigated the effects of lineage negative murine hematopoietic stem/progenitor cells (HSPCs) on the cerebral microcirculation following ischemia-reperfusion injury (I/RI). Following subsequent evaluation of the mRNA transcriptome of the explanted HSPCs, we assessed whether metallothionein (MT)-1, (increased in explanted HSPCs from I/R mice) administration was able to evoke similar neuro-protection following cerebral I/RI. Methods and Results: Murine HSPCs administered intravenously 24 hours (h) post cerebral I/R were selectively recruited to the brain of I/RI mice. Mice treated with HSPCs displayed decreased disease severity for up to 2-weeks post cerebral I/R, as evidenced by decreased mortality rate, decreased infarct volume, improved functional outcome, reduced microglial activation and elevated plasma levels of anti-inflammatory interleukin-10. Using confocal intravital microscopy, we found that transplanted cells had emigrated into the brain parenchyma and that RNA-seq analysis of explanted HSPCs indicated significantly increased levels of metallothionein transcripts, in particular MT-1. We further determined that treatment of mice with MT-1 significantly reduced neurological score and IV. Conclusions: These studies provide further evidence for HSPCs as a promising therapeutic strategy in promoting repair following cerebral I/RI, potentially via a MT-1 mechanism. Overall design: Murine HSPCs were administered into mice with I/RI intravenously 24 hours post cerebral I/R and selectively recruited to the brain. RNA profiles of explanted HSPCs were determined by RNA sequencing.
Publication Title
Metallothionein I as a direct link between therapeutic hematopoietic stem/progenitor cells and cerebral protection in stroke.
Sample Metadata Fields
Specimen part, Cell line, Treatment, Subject
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Gene 2.1 ST Array (mogene21st)
Description
Leptospirosis is a neglected zoonotic disease of global importance. Despite its prevalence, pathogenesis is still poorly understood. Our aim was to discover transcripts responsable for pathogenicity of leptospirosis. We compared the transcriptome profiles of saprophyte, attenuated and virulent strain of Leptospira spp.
Publication Title
Transcriptome datasets of macrophages infected with different strains of <i>Leptospira</i> spp.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 9 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Pandemic influenza H1N1 (pdmH1N1) virus causes mild disease in humans but occasionally leads to severe complications and even death, especially in those who are pregnant or have underlying disease. Cytokine responses induced by pdmH1N1 viruses in vitro are comparable to other seasonal influenza viruses, suggesting the cytokine dysregulation as seen in H5N1 infection is not a feature of the pdmH1N1 virus. However, a comprehensive gene expression profile of pdmH1N1 in relevant primary human cells in vitro has not been reported. Type I alveolar epithelial cells are a key target cell in pdmH1N1 pneumonia. We carried out a comprehensive gene expression profiling using the Affymetrix microarray platform to compare the transcriptomes of primary human alveolar type I-like alveolar epithelial cells infected with pdmH1N1 or seasonal H1N1 virus.
Publication Title
Systems-level comparison of host responses induced by pandemic and seasonal influenza A H1N1 viruses in primary human type I-like alveolar epithelial cells in vitro.
Sample Metadata Fields
Specimen part, Subject, Time
View Samples- Mus musculus
- 8 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Although heterochromatin is enriched with repressive traits, it is also actively transcribed, giving rise to large amounts of non-coding RNAs. Although these RNAs are responsible for the formation and maintenance of heterochromatin, little is known about how their transcription is regulated. Here we show that the Snail1 transcription factor represses pericentromeric transcription, acting through the H3K4 deaminase LOXL2. Since Snail1 plays a key role in the epithelial to mesenchymal transition (EMT), we analyzed the regulation of mouse heterochromatin transcription in this process. At the onset of EMT, one of the major structural heterochromatin proteins, HP1a, is transiently released from heterochromatin foci in a Snail1/LOXL2dependent manner during EMT, concomitantly with a down-regulation of major satellite transcription. Global transcriptome analysis indicated that ectopic expression of heterochromatin transcripts affects the transcription profile of EMT-related genes. Additionally, preventing the down-regulation of major satellite transcripts compromised the migratory and invasive behavior of mesenchymal cells. We propose that Snail1 regulates heterochromatin transcription through the histone-modifying enzyme, LOXL2, thus creating the favorable transcriptional state necessary for completing EMT.
Publication Title
Regulation of heterochromatin transcription by Snail1/LOXL2 during epithelial-to-mesenchymal transition.
Sample Metadata Fields
Cell line, Treatment
View Samples- Homo sapiens
- 21 Downloadable Samples
- Affymetrix Human Gene 2.0 ST Array (hugene20st)
Description
Avian influenza A (H7N9) viruses have emerged in China in 2013 and caused zoonotic disease associated with a case-fatality ratio of over 30%. Transcriptional profile from peripheral blood has been shown to reflect host responses against a specific respiratory pathogen and can be used to understand the disease. Methods: We correlated the clinical data and blood transcriptomic profile of patients with avian influenza A (H7N9) disease and determined the biological significance of the infection from the analysis.
Publication Title
Clinical Correlations of Transcriptional Profile in Patients Infected With Avian Influenza H7N9 Virus.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 8 Downloadable Samples
- Illumina HiSeq 2000
Description
The data was used to study mechanisms of apoptosis resistance induced by loss of PRC2. Overall design: CCRF-CEM cells infected with shLuciferase, shGFP, shEZH2.1, shEZH2.4, shEED2, shEED5, shSUZ12.2, shSUZ12.3 were harvested, RNA isolated, and RNAsequencing performed on HiSeq 2000.
Publication Title
PRC2 loss induces chemoresistance by repressing apoptosis in T cell acute lymphoblastic leukemia.
Sample Metadata Fields
Cell line, Subject
View Samples