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GSE54049
Arabidopsis thaliana
45 Downloadable Samples
Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)
Description
To identify potential transient interactions between a TF and its targets, we developed an approach that can identify primary targets based either on TF-induced regulation or TF-binding, assayed in the same samples. Our studies focused on the TF bZIP1 (BASIC LEUCINE ZIPPER 1), a central integrator of cellular and metabolic signaling.
Publication Title
Hit-and-run transcriptional control by bZIP1 mediates rapid nutrient signaling in Arabidopsis.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 29 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
As susceptibility to many adult disorders originates in utero, we here hypothesized that fetal sex influences gene expression in placental cells and produces functional differences in human placentas. We found that fetal sex differentially affects gene expression in a cell-phenotype dependent manner among all four placental cell-phenotypes studied: cytotrophoblasts, syncytiotrophoblasts, arterial endothelial cells and venous endothelial cells. The markedly enriched pathways in males were identified to be signaling pathways for graft-versus-host disease as well as the immune and inflammatory systems, both supporting the hypothesis that there is reduced maternal-fetal compatibility for male fetuses.
Publication Title
The human placental sexome differs between trophoblast epithelium and villous vessel endothelium.
Sample Metadata Fields
Sex, Specimen part
View Samples- Homo sapiens
- 22 Downloadable Samples
- Affymetrix Human Gene 1.1 ST Array (hugene11st)
Description
Relapse, associated with therapy resistance, is a major clinical problem in acute myeloid leukemia (AML), yet little is known about the underlying molecular mechanisms. Using genome wide gene expression profiling on 11 paired samples from diagnosis and relapse, we show that the expression of a substantial number of genes was altered in a highly consistent manner between these disease stages. Furthermore, the relapse associated gene expression profile was significantly enriched for leukemia stem cell (LSC) genes, indicating that recurring AML is characterized by increased stemness, and supporting the concept that it is due to the outgrowth of chemotherapy resistant LSCs.
Publication Title
A gene expression profile associated with relapse of cytogenetically normal acute myeloid leukemia is enriched for leukemia stem cell genes.
Sample Metadata Fields
Sex, Age
View Samples- Homo sapiens
- 12 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
To investigate whether and how expression of the oncogenic transcription factor EVI1 influences gene regulation by phorbol esters and vice versa, the human myeloid cell line U937 was transduced with an EVI1 expression vector or empty vector as a control. Cells were treated with 12-Otetradecanoylphorbol 13-acetate (TPA) or its solvent ethanol as a control. RNA was extracted and subjected to gene expression microarray analysis.
Publication Title
The oncogene EVI1 enhances transcriptional and biological responses of human myeloid cells to all-trans retinoic acid.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 10 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
The product of the ecotropic virus integration site 1 (EVI1) gene, whose overexpression is associated with a poor prognosis in myeloid leukemias and some epithelial tumors, regulates gene transcription both through direct DNA binding and through modulation of the activity of other sequence specific transcription factors. Previous results from our laboratory have shown that EVI1 influenced transcription regulation in response to the myeloid differentiation inducing agent, all-trans retinoic acid (ATRA), in a dual manner: it enhanced ATRA induced transcription of the RARb gene, but repressed the ATRA induction of the EVI1 gene itself. In the present study, we asked whether EVI1 would modulate the ATRA regulation of a larger number of genes, as well as biological responses to this agent, in human myeloid cells. U937 and HL-60 cells ectopically expressing EVI1 through retroviral transduction were subjected to microarray based gene expression analysis, and to assays measuring cellular proliferation, differentiation, and apoptosis. These experiments showed that EVI1 modulated the ATRA response of several dozens of genes, and in fact reinforced it in the vast majority of cases. A particularly strong synergy between EVI1 and ATRA was observed for GDF15, which codes for a member of the TGF-b superfamily of cytokines. In line with the gene expression results, EVI1 enhanced cell cycle arrest, differentiation, and apoptosis in response to ATRA, and knockdown of GDF15 counteracted some of these effects.
Publication Title
The oncogene EVI1 enhances transcriptional and biological responses of human myeloid cells to all-trans retinoic acid.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 10 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
The product of the ecotropic virus integration site 1 (EVI1) gene, whose overexpression is associated with a poor prognosis in myeloid leukemias and some epithelial tumors, regulates gene transcription both through direct DNA binding and through modulation of the activity of other sequence specific transcription factors. Previous results from our laboratory have shown that EVI1 influenced transcription regulation in response to the myeloid differentiation inducing agent, all-trans retinoic acid (ATRA), in a dual manner: it enhanced ATRA induced transcription of the RARb gene, but repressed the ATRA induction of the EVI1 gene itself. In the present study, we asked whether EVI1 would modulate the ATRA regulation of a larger number of genes, as well as biological responses to this agent, in human myeloid cells. U937 and HL-60 cells ectopically expressing EVI1 through retroviral transduction were subjected to microarray based gene expression analysis, and to assays measuring cellular proliferation, differentiation, and apoptosis. These experiments showed that EVI1 modulated the ATRA response of several dozens of genes, and in fact reinforced it in the vast majority of cases. A particularly strong synergy between EVI1 and ATRA was observed for GDF15, which codes for a member of the TGF-b superfamily of cytokines. In line with the gene expression results, EVI1 enhanced cell cycle arrest, differentiation, and apoptosis in response to ATRA, and knockdown of GDF15 counteracted some of these effects.
Publication Title
The oncogene EVI1 enhances transcriptional and biological responses of human myeloid cells to all-trans retinoic acid.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 22 Downloadable Samples
Ion Torrent Proton
Description
We designed a study to investigate immunoediting of an epithelial cancer genome using wildtype and immunodeficient mice, NGS, and analytical pipelines to process and analyze the data. We carried out experiments with wildtype and immunodeficient RAG1-/- mice with transplanted tumors and analyzed longitudinal samples with respect to the genomic landscape and the immunophenotypes of the tumors. Finally, we performed also experiments with anti-PD-L1 antibodies and show how the activation of the PD1-PD-L1 axis modulates immunoediting. MC38 cells were subcutaneously injected into wild-type C57Bl/6 and immunodeficient Rag1-/- mice. Samples were taken at predefined time points and subjected to detailed analysis, including FACS, exome sequencing, RNA sequencing and SNP arrays. Overall design: Samples were taken at predifined time points, in triplicates and subjected to RNA sequencing using Ion Torrent Proton
Publication Title
Targeting immune checkpoints potentiates immunoediting and changes the dynamics of tumor evolution.
Sample Metadata Fields
Subject, Time
View Samples- Homo sapiens
- 15 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Background: The main focus of the work was the evaluation of gene expression differences between our established NSCLC 3D cell culture model and the 2D cell culture in regard to the use of our model for drug screening applications.
Publication Title
3D-cultivation of NSCLC cell lines induce gene expression alterations of key cancer-associated pathways and mimic <i>in-vivo</i> conditions.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 86 Downloadable Samples
- Affymetrix Human Full Length HuGeneFL Array (hu6800), Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Disparate Oxidant-related Gene Expression of Human Small Airway Epithelium Compared to Autologous Alveolar Macrophages in Response to the In Vivo Oxidant Stress of Cigarette Smoking
Publication Title
Disparate oxidant gene expression of airway epithelium compared to alveolar macrophages in smokers.
Sample Metadata Fields
Sex, Age
View Samples- Homo sapiens
- 220 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Cystatin A (gene: CSTA), is up-regulated in non-small-cell lung cancer (NSCLC) and dysplastic vs normal human bronchial epithelium. In the context that chronic obstructive pulmonary disease (COPD), a small airway epithelium (SAE) disorder, is independently associated with NSCLC (especially squamous cell carcinoma, SCC), but only occurs in a subset of smokers, we hypothesized that genetic variation, smoking and COPD modulate CSTA gene expression levels in SAE, with further up-regulation in SCC. Gene expression was assessed by microarray in SAE of 178 individuals [healthy nonsmokers (n=60), healthy smokers (n=82), and COPD smokers (n=36)], with corresponding large airway epithelium (LAE) data in a subset (n=52). Blood DNA was genotyped by SNP microarray. Twelve SNPs upstream of the CSTA gene were all significantly associated with CSTA SAE gene expression (p<0.04 to 5 x 10-4). CSTA gene expression levels in SAE were higher in COPD smokers (28.4 2.0) than healthy smokers (19.9 1.4, p<10-3), who in turn had higher levels than nonsmokers (16.1 1.1, p<0.04). CSTA LAE gene expression was also smoking-responsive (p<10-3). Using comparable publicly available NSCLC expression data, CSTA was up-regulated in SCC vs LAE (p<10-2) and down-regulated in adenocarcinoma vs SAE (p<10-7). All phenotypes were associated with significantly different proportional gene expression of CSTA to cathepsins. The data demonstrate that regulation of CSTA expression in human airway epithelium is influenced by genetic variability, smoking, and COPD, and is further up-regulated in SCC, all of which should be taken into account when considering the role of CSTA in NSCLC pathogenesis.
Publication Title
Modulation of cystatin A expression in human airway epithelium related to genotype, smoking, COPD, and lung cancer.
Sample Metadata Fields
Race
View Samples