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SRP004454
Drosophila melanogaster
3 Downloadable Samples
Illumina Genome Analyzer II
Description
MSL (Male-specific lethal) complex increases transcription on the single X chromosome of Drosophila males in order to equalize expression of X-linked genes between males (XY) and females (XX). The increase in transcript levels correlates with MSL- dependent acetylation of histone H4 at K16 within the bodies of active genes, but identification of the transcriptional step affected has not been possible. In this study, we use global run-on sequencing (GRO-seq) to examine the specific effect of MSL complex on RNA Polymerase II (RNAP II) on a genome-wide level. Results indicate that MSL complex enhances transcription by facilitating the progression of RNAP II across the bodies of active X-linked genes. Improving transcriptional output downstream of typical gene-specific control may explain how dosage compensation can be imposed on the diverse set of genes along an entire chromosome. Overall design: Global Run-On Sequencing (GRO-Seq) reads, i.e., RNA-Seq of nascent RNA transcripts, from D. Melanogaster SL2 cells. Two biological replicates were analyzed.
Publication Title
Comprehensive analysis of the chromatin landscape in Drosophila melanogaster.
Sample Metadata Fields
Subject
View Samples- Homo sapiens
- 117 Downloadable Samples
Illumina HumanHT-12 V3.0 expression beadchip
Description
Background: Gene expression profiling has shown its ability to identify with high accuracy low cytogenetic risk acute myeloid leukemia such as acute promyelocytic leukemia and leukemias with t(8;21) or inv(16). The aim of this gene expression profiling study was to evaluate to what extent suboptimal samples with low leukemic blast load (range, 2-59%) and/or poor quality control criteria could also be correctly identified. Methods: Specific signatures were first defined so that all 71 acute promyelocytic leukemia, leukemia with t(8;21) or inv(16)-AML as well as cytogenetically normal acute myeloid leukemia samples with at least 60% blasts and good quality control criteria were correctly classified (training set). The classifiers were then evaluated for their ability to assign to the expected class 111 samples considered as suboptimal because of a low leukemic blast load (n=101) and/or poor quality control criteria (n=10) (test set). Results: With 10-marker classifiers, all training set samples as well as 97 of the 101 test samples with a low blast load, and all 10 samples with poor quality control criteria were correctly classified. Regarding test set samples, the overall error rate of the class prediction was below 4 percent, even though the leukemic blast load was as low as 2%. Sensitivity, specificity, negative and positive predictive values of the class assignments ranged from 91% to 100%. Of note, for acute promyelocytic leukemia and leukemias with t(8;21) or inv(16), the confidence level of the class assignment was influenced by the leukemic blast load. Conclusion: Gene expression profiling and a supervised method requiring 10-marker classifiers enable the identification of favorable cytogenetic risk acute myeloid leukemia even when samples contain low leukemic blast loads or display poor quality control criterion.
Publication Title
Routine use of microarray-based gene expression profiling to identify patients with low cytogenetic risk acute myeloid leukemia: accurate results can be obtained even with suboptimal samples.
Sample Metadata Fields
Time
View Samples- Homo sapiens
- 27 Downloadable Samples
- Illumina HumanHT-12 V3.0 expression beadchip
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Routine use of microarray-based gene expression profiling to identify patients with low cytogenetic risk acute myeloid leukemia: accurate results can be obtained even with suboptimal samples.
Sample Metadata Fields
Specimen part, Time
View Samples- Mus musculus
- 22 Downloadable Samples
- Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
The NAT enzymes are polymorphic xenobiotic metabolizing enzymes that catalyze the transfer of an acetyl moiety from acetyl coenzyme A (acetyl-CoA) to the nitrogen or oxygen atom of primary arylamines, hydrazines, and their N-hydroxylated metabolites. NATs therefore play an important role in the detoxification and/or activation of arylamine drugs and carcinogens. The involvement of acetyl-CoA in energy metabolism suggests that there may be relationships between NAT activity and energy metabolism. Previous studies have suggested a role for NAT2 in insulin sensitivity that is exacerbated on high fat diet, using Nat1 knockout mice. To study mice with no NAT activity at all, we used a Nat1/Nat2 double-KO model, with animals fed either a regular chow or high fat/high sugar diet for 12 weeks. Analysis of basal parameters suggested a decrease in fatty-acid oxidation and hepatic gluconeogenesis. To further evaluate the cause of this, RNA was isolated and processed using Affymetrix Mouse Gene 2.0 microarrays.
Publication Title
A readout of metabolic efficiency in arylamine N-acetyltransferase-deficient mice reveals minor energy metabolism changes.
Sample Metadata Fields
Sex
View Samples- Mus musculus
- 4 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Mice knocked-out or wild type for the NAPE PLD gene specifically in adipose tissue, were recruited for this expression profiling experiment. Each group of mice (WT versus cKO) were fed with a control diet or a high fat diet. Then mice were sacrificed and adipose tissue samples form the subcutaneous adipose tissue were processed for RNA extraction. Total RNA of each sample was then pooled with those of the same group and treatment for microarray hybridization.
Publication Title
Adipose tissue NAPE-PLD controls fat mass development by altering the browning process and gut microbiota.
Sample Metadata Fields
Age, Specimen part
View Samples- Homo sapiens
- 50 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
HER2 is a tyrosine kinase receptor causally involved in cancer. A subgroup of breast cancer patients with particularly poor clinical outcome expresses a heterogeneous collection of HER2 carboxy-terminal fragments (CTFs). However, since the CTFs lack the extracellular domain that drives dimerization and subsequent activation of full-length HER2, they are in principle expected to be inactive. Here we present evidence that at low expression levels one of these fragments, 611-CTF, activated multiple signaling pathways because of its unanticipated ability to constitutively homodimerize. A transcriptomic analysis revealed that 611-CTF specifically controlled the expression of genes that we found correlated with poor prognosis in breast cancer. Among the 611-CTF-regulated genes were several that previously have been linked to metastasis, including MET, EPHA2, MMP1, IL11, ANGPTL4 and different Integrins. Transgenic mice overexpressing HER2 in the mammary gland develop tumors only after acquisition of activating mutations in the transgene. In contrast, we show that expression of 611-CTF led to development of aggressive and invasive mammary tumors without the need for mutations. These results demonstrate that 611-CTF is a potent oncogene capable of promoting mammary tumor progression and metastasis.
Publication Title
A naturally occurring HER2 carboxy-terminal fragment promotes mammary tumor growth and metastasis.
Sample Metadata Fields
Cell line, Time
View Samples- Homo sapiens
- 118 Downloadable Samples
- Affymetrix Human Transcriptome Array 2.0 (hta20)
Description
Triple negative breast cancer is a heterogeneous disease with distinct molecular subtypes that differentially respond to chemotherapy and targeted agents. The purpose of this study was to explore the clinical relevance of Lehmann triple negative breast cancer subtypes by identifying any differences in response to neoadjuvant chemotherapy among them.
Publication Title
Triple negative breast cancer subtypes and pathologic complete response rate to neoadjuvant chemotherapy.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Mus musculus
- 10 Downloadable Samples
- NextSeq 500
Description
Microglia constitutes a diverse population of cells that present a broad spectrum of responses when they become activated. Here, microglial status was studied under steady-state conditions from different brain regions involved in neurodegenerative diseases. Under basal conditions, midbrain microglia showed an immune-alert state not observed in striatum. Unique subpopulations of microglia expressing TLR4 and MHC-II with antigen presenting properties, and a higher proportion of infiltrating CD4+ T cells were identified in the midbrain. These results highlight that the inflammatory tone is context-dependent and reveal the unique properties of the midbrain related to the interaction with the immune system. Overall design: Analysis of two cohorts of control animals
Publication Title
Midbrain microglia mediate a specific immunosuppressive response under inflammatory conditions.
Sample Metadata Fields
Age, Cell line, Subject
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
We propose the hypothesis that loss of estrogen receptor function which leads to endocrine resistance in breast cancer, also results in de-differentiation from an epithelial to a mesenchymal phenotype that is responsible for increased aggressiveness and metastatic propensity. siRNA mediated silencing of the estrogen receptor in MCF7 breast cancer cells resulted in estrogen/tamoxifen resistant cells (pII) with altered morphology, increased motility with rearrangement and switch from an actin to a vimentin based cytoskeleton, and ability to invade simulated components of the extracellular matrix. Phenotypic profiling using an Affymetrix Human Genome U133 plus 2.0 GeneChip indicated fold changes 3 in approximately 2500 identifiable unique sequences, with about 1270 of these being up-regulated in pII cells. Changes were associated with genes whose products are involved in cell motility, loss of cellular adhesion and interaction with the extracellular matrix. Selective analysis of the data also showed a shift from luminal to basal cell markers and increased expression of a wide spectrum of genes normally associated with mesenchymal characteristics, with consequent loss of epithelial specific markers. Over-expression of several peptide growth factors and their receptors are indicative of an increased contribution to the higher proliferative rates of pII cells as well as aiding their potential for metastatic activity. Signalling molecules that have been identified as key transcriptional drivers of epithelial to mesenchymal transition were also found to be elevated in pII cells. We suggest that these data support our hypothesis that induced loss of estrogen receptor in previously antiestrogen sensitive cells is a trigger for the concomitant loss of endocrine dependence and onset of a series of possibly parallel events that changes the cell from an epithelial to a mesenchymal type. Inhibition of this transition through targeting of specific mediators may be a useful supplementary strategy to circumvent the effects of loss of endocrine sensitivity.
Publication Title
Estrogen receptor silencing induces epithelial to mesenchymal transition in human breast cancer cells.
Sample Metadata Fields
Cell line
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